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1. 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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2. 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


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


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

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  • (PMID = 17852433.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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6. Wodarz D: Stem cell regulation and the development of blast crisis in chronic myeloid leukemia: Implications for the outcome of Imatinib treatment and discontinuation. Med Hypotheses; 2008;70(1):128-36
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  • [Title] Stem cell regulation and the development of blast crisis in chronic myeloid leukemia: Implications for the outcome of Imatinib treatment and discontinuation.
  • Chronic myeloid leukemia (CML) is a cancer of the hematopoietic system that is initiated by a single genetic alteration (the BCR-ABL fusion gene or Philadelphia chromosome) and progresses in several phases: during the chronic phase the number of cells grows slowly and the fraction of immature cells is low.
  • During the accelerated phase and blast crisis, the population of CML cells and the fraction of immature cells rises sharply.
  • The mechanisms that drive the transition from the chronic phase to blast crisis are not understood, and the requirement of genetic instability and further mutations has been suggested.
  • Using mathematical models, I describe a theory that can account for the transition from the chronic phase to blast crisis without the need to invoke further mutations.
  • According to the model, treatment can lead to the low level persistence of CML stem cells without assuming that these cells are less susceptible to drug-mediated activity, and this might explain why disease tends to relapse after treatment discontinuation even in the absence of acquired drug resistance.
  • Further, the model defines conditions when Imatinib treatment might lead to the eradication of CML, which is relevant in the context of recent data that show absence of relapse as long as two years after treatment cessation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blast Crisis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Cell Division / drug effects. Disease Progression. Drug Administration Schedule. Humans. Imatinib Mesylate. Models, Biological. Stem Cells / pathology


7. Quintás-Cardama A, Kantarjian H, O'brien S, Borthakur G, Bruzzi J, Munden R, Cortes J: Pleural effusion in patients with chronic myelogenous leukemia treated with dasatinib after imatinib failure. J Clin Oncol; 2007 Sep 1;25(25):3908-14
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  • [Title] Pleural effusion in patients with chronic myelogenous leukemia treated with dasatinib after imatinib failure.
  • PURPOSE: We investigated the risk factors and management of pleural effusion associated with dasatinib therapy for chronic myelogenous leukemia (CML) after failure of imatinib.
  • PATIENTS AND METHODS: We analyzed 138 patients with CML treated with dasatinib from November 2003 to January 2006 in one phase I (n = 50) and four phase II (n = 88) studies for the development of pleural effusion.
  • RESULTS: Pleural effusion occurred in 48 patients (35%; grade 3/4 in 23 [17%]), including 29% of those treated in chronic phase (CP), 50% in accelerated phase (AP), and 33% in blast phase (BP).
  • By multivariate analysis, history of cardiac disease, hypertension, and use of a twice-daily schedule (v once daily) were identified as factors associated with development of pleural effusions.
  • A twice-daily schedule may result in a higher incidence of pleural effusion.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pleural Effusion / chemically induced. Pyrimidines / adverse effects. Pyrimidines / therapeutic use. Thiazoles / adverse effects. Thiazoles / therapeutic use

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  • (PMID = 17761974.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
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8. Oztop I, Yaren A, Demirpence M, Alacacioglu I, Tuna B, Piskin O, Yilmaz U: The development of metachronous prostate cancer and chronic myeloid leukemia in a patient with metastatic rectal cancer. J BUON; 2008 Apr-Jun;13(2):267-70
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  • [Title] The development of metachronous prostate cancer and chronic myeloid leukemia in a patient with metastatic rectal cancer.
  • We report herein an unusual case of metachronous triple cancers (rectum, prostate and Philadelphia(+) [Ph(+)] chronic myeloid leukemia [CML]).
  • A metastatic rectal cancer was diagnosed in a 76-year-old male patient, who was treated with transanal tumor resection and chemotherapy.
  • Thirty months from the initial rectal cancer diagnosis, prostate cancer was diagnosed and the patient was administered maximal androgen blockade and received palliative radiotherapy to the lumbar spine because of painful bone metastases.
  • Thirty months after the diagnosis of rectal cancer and 12 months after the diagnosis of prostate cancer the patient developed Ph(+) CML and imatinib treatment was started.
  • After one-year period in remission, CML evolved into accelerated phase and the patient died of intracranial hemorrhage.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Neoplasms, Multiple Primary / pathology. Prostatic Neoplasms / pathology. Rectal Neoplasms / pathology. Stomach Neoplasms / pathology


9. Kaygusuz G, Kuzu I, Akpınar E, Uysal A: Extramedullary hematopoiesis in the axillary lymph node in a patient with an accelerated phase of chronic myeloid leukemia. Turk J Haematol; 2009 Mar 5;26(1):40-1
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  • [Title] Extramedullary hematopoiesis in the axillary lymph node in a patient with an accelerated phase of chronic myeloid leukemia.

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  • (PMID = 27265110.001).
  • [ISSN] 1300-7777
  • [Journal-full-title] Turkish journal of haematology : official journal of Turkish Society of Haematology
  • [ISO-abbreviation] Turk J Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
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10. 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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11. Chen ZC, You Y, Zhu XM, Li QB, Li WM, Zou P: [A clinical study of treating 120 cases of adult chronic myelocytic leukemia with imatinib mesylate]. Zhonghua Nei Ke Za Zhi; 2007 Dec;46(12):1003-6
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  • [Title] [A clinical study of treating 120 cases of adult chronic myelocytic leukemia with imatinib mesylate].
  • OBJECTIVE: To analyze and evaluate the clinical efficacy and safety of imatinib mesylate (IM) as a tyrosine kinase inhibitor on Ph-positive or BCR/ABL positive chronic myelogenous leukemia (CML).
  • METHODS: 120 patients diagnosed as CML with positive Ph chromosome were treated with IM 400 mg/d for CML in chronic phase (CP) (n = 90) or 600 mg/d for CML in accelerated or blastic phase (AP or BP) (n = 30) once daily.
  • Hematological, cytogenetic and molecular effects of IM on the disease process of these patients were evaluated with blood and marrow cells morphology examination, G-band conventional cytogenetics analysis for Ph chromosome and PCR assay for BCR/ABL gene.
  • (1) In CML-CP patients, after a follow-up of 9 ( range 3-42) months, cumulative complete hematological response (CHR), complete cytogenetic response (CCyR) and complete molecular response (CMR) rates were 73.3%, 66.7% and 54.4%, which was not influenced by prior treatment of interferon.
  • CMR was better when time from diagnosis to treatment with IM was < or = 6 months (P < 0.05).
  • It is significant that the time to first CHR and time to first CCyR were related with the time to first CCyR and the time to first negative BCR/ ABL, respectively (both P < 0.05), while there was no relation between the time to first CHR and the time to first negative BCR/ABL (P > 0.05). (2) CHR, CCyR and CMR rates of the patients with progressive course (AP and BP) were 43.3%, 25.9% and 25.0%, respectively.
  • CONCLUSION: IM can lead to considerable hematological, cytogenetic and molecular response rates in CML, especially CML-CP patients, with minor tolerable side effects.
  • [MeSH-major] Leukemia, Myeloid, Chronic-Phase / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Benzamides. Female. Fusion Proteins, bcr-abl / genetics. Humans. Imatinib Mesylate. Male. Middle Aged. Philadelphia Chromosome. Retrospective Studies. Treatment Outcome

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  • (PMID = 18478917.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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12. Yin CC, Abruzzo LV, Qiu X, Apostolidou E, Cortes JE, Medeiros LJ, Lu G: del(15q) is a recurrent minor-route cytogenetic abnormality in the clonal evolution of chronic myelogenous leukemia. Cancer Genet Cytogenet; 2009 Jul;192(1):18-23
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  • [Title] del(15q) is a recurrent minor-route cytogenetic abnormality in the clonal evolution of chronic myelogenous leukemia.
  • The del(15q) chromosomal abnormality is known to occur in acute leukemias, but has rarely been described in chronic myelogenous leukemia (CML).
  • Described here are five cases of CML associated with del(15q): four men and one woman.
  • Bone marrow aspirate smears showed increased blasts in all cases at the time of del(15q) detection, in accelerated phase in two cases and myeloid blast phase in three.
  • Of the three patients who did not receive ASCT, one died, one was in persistent blast phase, and one was in clinical remission with molecular evidence of residual disease at 16, 6, and 34 months, respectively, after identification of the del(15q).
  • Of the two patients who had ASCT, one died and one was in clinical remission with molecular evidence of disease at 15 and 64 months, respectively, after identification of the del(15q).
  • These findings indicate that del(15q) is a recurrent cytogenetic abnormality that may be seen at initial presentation of advanced disease or may emerge during disease progression.
  • Del(15q) appears to be associated with a poor prognosis in CML.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 15. Clone Cells / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics

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  • (PMID = 19480932.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS627187; NLM/ PMC4167428
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13. Hochhaus A, O'Brien SG, Guilhot F, Druker BJ, Branford S, Foroni L, Goldman JM, Müller MC, Radich JP, Rudoltz M, Mone M, Gathmann I, Hughes TP, Larson RA, IRIS Investigators: Six-year follow-up of patients receiving imatinib for the first-line treatment of chronic myeloid leukemia. Leukemia; 2009 Jun;23(6):1054-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Six-year follow-up of patients receiving imatinib for the first-line treatment of chronic myeloid leukemia.
  • Imatinib mesylate is considered standard of care for first-line treatment of chronic phase chronic myeloid leukemia (CML-CP).
  • In the phase III, randomized, open-label International Randomized Study of Interferon vs STI571 (IRIS) trial, previously untreated CML-CP patients were randomized to imatinib (n=553) or interferon-alpha (IFN) plus cytarabine (n=553).
  • This 6-year update focuses on patients randomized to receive imatinib as first-line therapy for newly diagnosed CML-CP.
  • During the sixth year of study treatment, there were no reports of disease progression to accelerated phase (AP) or blast crisis (BC).
  • The estimated overall survival was 88% -- or 95% when only CML-related deaths were considered.
  • This 6-year update of IRIS underscores the efficacy and safety of imatinib as first-line therapy for patients with CML.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Benzamides. Disease Progression. Follow-Up Studies. Heart Failure / chemically induced. Humans. Imatinib Mesylate. Neoplasms, Second Primary / chemically induced. Remission Induction. Survival Analysis. Treatment Outcome

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  • [ErratumIn] Leukemia. 2010 May;24(5):1102
  • (PMID = 19282833.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Investigator] Hughes T; Taylor K; Durant S; Schwarer A; Joske D; Seymour J; Grigg A; Ma D; Arthur C; Bradstock K; Joshua D; Agis H; Verhoef G; Louwagie A; Martiat P; Bosly A; Shepherd J; Shistok C; Lipton J; Forrest D; Walker I; Roy DC; Rubinger M; Bence-Bruckler I; Stewart D; Kovacs M; Turner AR; Nielsen J; Birgens H; Bjerrum O; Rousselot P; Reiffers J; Facon T; Harousseau JL; Tulliez M; Guerci A; Blaise D; Maloisel F; Michallet M; Fischer T; Hochhaus A; Andreesen R; Nerl C; Freund M; Gattermann N; Ehninger G; Niederwieser D; Ottmann OG; Peschel C; Ho AD; Neubauer A; le Coutre P; Aulitzky W; Saglio G; Baccarani M; Fanin R; Rosti G; Mandelli F; Lazzarino M; Morra E; Carella A; Petrini M; Nobile F; Liso V; Ferrara F; Rizzoli V; Fiortoni G; Martinelli G; Cornelissen J; Ossenkoppele G; Browett P; Gedde-Dahl T; Tangen JM; Dahl I; Cervantes F; Odrizoala J; Hernandez Boulda JC; Steegmann JL; Canizo C; Diaz J; Grenena A; Fernandez M; Simonsson B; Stenke L; Paul C; Bjoreman M; Malm C; Wadenvik H; Nilsson PG; Turesson I; Gratwohl A; Hess U; Solenthaler M; Goldman JM; Clark RE; Green A; Holyoake T; Lucas G; Smith G; Milligan D; Rule S; Burnett A; Kantarjian H; Silver R; Stone R; Powell B; Gabrilove J; Moroose R; Wetzler M; Bearden J; Cataland S; Rabinowitz I; Meisenberg B; Thompson K; Graziano S; Emanuel P; Gross H; Cobb P; Bhatia R; Dakhil S; Irwin AD; Issell B; Pavletic S; Kuebler P; Layhe E; Butra P; Glass J; Moore J; Grant B; Neill H; Herzig R; Burris H; Petersen B; Kalaycio M; Stirewalt D; Samlowski W; Berman E; Limentani S; Seay T; Shea T; Akard L; Smith G; Becker P; Devine S; Hart R; Veith R; Wade J; Brunvad M; Kalman L; Strickland D; Shurafa M; Bashey A; Shadduck R; Safah H; Rubenstein M; Collins R; Keller A; Tallman M; Pecora A; Agha M; Homes H; Guidice R; Druker BJ; Guilhot F; Larson RA; O'Brien S; Rowe J; Schiffer CA; Buyse M; Baccarani M; Cervantes F; Cornelissen J; Fischer T; Hochhaus A; Hughes T; Lechner K; Nielsen JL; Reiffers J; Rousselot P; Saglio G; Shepherd J; Simonsson B; Gratwohl A; Goldman JM; Talpaz M; Taylor K; Verhoef G; Santini V
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14. Valent P, Agis H, Sperr W, Sillaber C, Horny HP: Diagnostic and prognostic value of new biochemical and immunohistochemical parameters in chronic myeloid leukemia. Leuk Lymphoma; 2008 Apr;49(4):635-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnostic and prognostic value of new biochemical and immunohistochemical parameters in chronic myeloid leukemia.
  • Chronic myeloid leukemia (CML) is a stem-cell disease characterized by multilineage expansion of clonal BCR/ABL+ cells.
  • Transformation from chronic into accelerated and blast phase of CML is usually associated with drug resistance and is accompanied by typical clinical and/or laboratory features, such as splenomegaly, increase in precursor cells, disturbed megakaryopoiesis, basophilia or marrow fibrosis.
  • Because of new treatment options, early recognition of disease-acceleration is of importance.
  • These tests are useful to quantitate basophil-lineage cells in the peripheral blood in CML, to determine and quantify basophilia in the bone marrow, and to detect focal accumulations of blast cells and megakaryocytes as well as increased angiogenesis and fibrosis in bone marrow sections.
  • Application of these markers may assist in determining the phase of disease and may help to better predict the prognosis in individual patients.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis


15. Silver RT, Cortes J, Waltzman R, Mone M, Kantarjian H: Sustained durability of responses and improved progression-free and overall survival with imatinib treatment for accelerated phase and blast crisis chronic myeloid leukemia: long-term follow-up of the STI571 0102 and 0109 trials. Haematologica; 2009 May;94(5):743-4
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  • [Title] Sustained durability of responses and improved progression-free and overall survival with imatinib treatment for accelerated phase and blast crisis chronic myeloid leukemia: long-term follow-up of the STI571 0102 and 0109 trials.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Benzamides. Blast Crisis / drug therapy. Blast Crisis / pathology. Clinical Trials, Phase II as Topic. Disease-Free Survival. Follow-Up Studies. Humans. Imatinib Mesylate. Leukemia, Myeloid, Accelerated Phase / drug therapy. Leukemia, Myeloid, Accelerated Phase / pathology. Treatment Outcome


16. Gucluler G, Baran Y: Docetaxel enhances the cytotoxic effects of imatinib on Philadelphia positive human chronic myeloid leukemia cells. Hematology; 2009 Jun;14(3):139-44
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  • [Title] Docetaxel enhances the cytotoxic effects of imatinib on Philadelphia positive human chronic myeloid leukemia cells.
  • Chronic myelogenous leukemia (CML) results from a translocation between chromosomes 9 and 22 which generates BCR/ABL fusion protein and characterized by uncontrolled proliferation of immature white blood cells.
  • Imatinib, a molecularly targeting anticancer agent, is used widely for the treatment of CML and showed significant activity in chronic and accelerated phases but much less in blast crisis phase.
  • The resistance to imatinib especially in blast crisis phase is recognized as a major problem in the treatment of CML patients.
  • Docetaxel is shown to arrest cells in G2/M phase of the cell cycle which makes cells more sensitive to chemo- and radiotherapy.
  • In this study, we aimed to increase chemosensitivity of human K562 CML cells to imatinib in combination with docetaxel.
  • Taken together, our results showed that the combination of imatinib and docetaxel decreased cellular proliferation and increased apoptosis in human K562 chronic myeloid leukemia cells as compared to any agent alone.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / pharmacology. Pyrimidines / pharmacology. Radiation-Sensitizing Agents / pharmacology. Taxoids / pharmacology

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  • (PMID = 19490758.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Radiation-Sensitizing Agents; 0 / Taxoids; 15H5577CQD / docetaxel; 8A1O1M485B / Imatinib Mesylate; EC 3.4.22.- / Caspase 3
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17. Ruiz-Argüelles GJ, Tarin-Arzaga LC, Gonzalez-Carrillo ML, Gutierrez-Riveroll KI, Rangel-Malo R, Gutiérrez-Aguirre CH, Cantú-Rodríguez OG, Gómez-Almaguer D, Giralt S: Therapeutic choices in patients with Ph-positive CML living in Mexico in the tyrosine kinase inhibitor era: SCT or TKIs? Bone Marrow Transplant; 2008 Jul;42(1):23-8
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  • [Title] Therapeutic choices in patients with Ph-positive CML living in Mexico in the tyrosine kinase inhibitor era: SCT or TKIs?
  • A total of 72 patients with Ph-positive CML in first chronic phase were followed during a 6-year period in two different institutions in México.
  • The freedom from progression to blast or accelerated phases was also similar for both groups, as well as the overall OS after diagnosis.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 18612313.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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18. 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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19. 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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20. Jørgensen HG, Copland M, Allan EK, Jiang X, Eaves A, Eaves C, Holyoake TL: Intermittent exposure of primitive quiescent chronic myeloid leukemia cells to granulocyte-colony stimulating factor in vitro promotes their elimination by imatinib mesylate. Clin Cancer Res; 2006 Jan 15;12(2):626-33
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  • [Title] Intermittent exposure of primitive quiescent chronic myeloid leukemia cells to granulocyte-colony stimulating factor in vitro promotes their elimination by imatinib mesylate.
  • PURPOSE: Primitive quiescent chronic myeloid leukemia (CML) cells are biologically resistant to imatinib mesylate, an inhibitor of the p210(BCR-ABL) kinase.
  • EXPERIMENTAL DESIGN: CD34(+) leukemic cells were isolated from six newly diagnosed chronic phase CML patients and cultured for 12 days in serum-free medium with or without G-CSF and/or imatinib mesylate present either continuously or intermittently (three cycles of G-CSF for 0, 1, or 4 days +/- imatinib mesylate for 0, 3, or 4 days).
  • RESULTS: Intermittent but not continuous exposure to G-CSF significantly accelerated the disappearance in vitro of initially quiescent CD34(+) CML cells.
  • CONCLUSION: Intermittent exposure to G-CSF can enhance the effect of imatinib mesylate on CML cells by specifically targeting the primitive quiescent leukemic elements.
  • A protocol for treating chronic-phase CML patients with imatinib mesylate that incorporates intermittent G-CSF exposure may offer a novel strategy for obtaining improved responses in vivo.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Marrow Cells / drug effects. Granulocyte Colony-Stimulating Factor / administration & dosage. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Blast Crisis. Culture Media, Serum-Free / pharmacology. Drug Combinations. Fusion Proteins, bcr-abl / metabolism. Humans. Imatinib Mesylate. In Vitro Techniques. Protein-Tyrosine Kinases / antagonists & inhibitors. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Granulocyte Colony-Stimulating Factor / genetics. Receptors, Granulocyte Colony-Stimulating Factor / metabolism. Tumor Cells, Cultured

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  • (PMID = 16428509.001).
  • [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
  • [Grant] United Kingdom / Medical Research Council / / G84/6317; United Kingdom / Chief Scientist Office / / SCD/04
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Culture Media, Serum-Free; 0 / Drug Combinations; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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21. Hughes T, Saglio G, Branford S, Soverini S, Kim DW, Müller MC, Martinelli G, Cortes J, Beppu L, Gottardi E, Kim D, Erben P, Shou Y, Haque A, Gallagher N, Radich J, Hochhaus A: Impact of baseline BCR-ABL mutations on response to nilotinib in patients with chronic myeloid leukemia in chronic phase. J Clin Oncol; 2009 Sep 01;27(25):4204-10
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  • [Title] Impact of baseline BCR-ABL mutations on response to nilotinib in patients with chronic myeloid leukemia in chronic phase.
  • PURPOSE: Nilotinib is a second-generation tyrosine kinase inhibitor indicated for the treatment of patients with chronic myeloid leukemia (CML) in chronic phase (CP; CML-CP) and accelerated phase (AP; CML-AP) who are resistant to or intolerant of prior imatinib therapy.
  • In this subanalysis of a phase II study of nilotinib in patients with imatinib-resistant or imatinib-intolerant CML-CP, the occurrence and impact of baseline and newly detectable BCR-ABL mutations were assessed.
  • PATIENTS AND METHODS: Baseline mutation data were assessed in 281 (88%) of 321 patients with CML-CP in the phase II nilotinib registration trial.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Mutation. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use


22. Xing W, Gu BW, Zhu YM, Jiang CL, Zhao RH, Wang AH, Sun HP, Li JM, Shen ZX, Chen Z, Chen SJ: [Detection and quantification of BCR-ABL transcripts in patients with chronic myeloid leukemia by real-time quantitative reverse transcriptase polymerase chain reaction]. Zhonghua Yi Xue Za Zhi; 2005 Feb 23;85(7):453-7
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  • [Title] [Detection and quantification of BCR-ABL transcripts in patients with chronic myeloid leukemia by real-time quantitative reverse transcriptase polymerase chain reaction].
  • OBJECTIVE: To investigate the effect of real-time quantitative reverse transcriptase polymerase chain reaction (RT-PCR) approach in chronic myeloid leukemia (CML) for detecting the minimal residual disease (MRD) or monitoring the treatment response and predicting the prognosis.
  • METHODS: Fifty-six CML patients, 39 males and 17 females, aged 39 (16 approximately 66), with disease history and frozen RNA specimens were studied, 31 of which were in the incipient chronic phase, 7 in the accelerated phase, and 17 in the rapidly progressing phase.
  • Breakpoint cluster region-Abelson murine leukemia viral oncogene (BCR-ABL) of the patients in different CML stages was analyzed by RT-PCR approach.
  • RESULTS: The BCR-ABL transcript of those patients remaining in chronic period after treatment decreased to 1/3 that of the baseline level six months after the initiation of treatment and then remained at that level.
  • The BCR-ABL transcript of those in which progressing change occurred increased when such change occurred.
  • After allogeneic transplantation of peripheral blood stem cells the BCR-ABL level decreased significantly.
  • The median DoseN in the 17 progressing patients was 10 492, significantly higher than those of the 31 patients in chronic phase (5920) and in the 7 patients in accelerated phase (4444, both P < 0.05).
  • The minimal residual disease and the treatment response were closely associated with the level and its variation of BCR-ABL transcripts, the transcripts level in blastic crisis was significantly higher than that in chronic phase or accelerated phase.
  • CONCLUSION: Real-time quantitative RT-PCR is reliable and can be used to detect the minimal residual disease, monitor the treatment outcome, and predicting blastic crisis.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use


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

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  • (PMID = 15671523.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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24. Anand M, Ghara N, Kumar R, Singh S, Sengar M, Panikar N, Raina V, Sharma A: Myeloperoxidase cytochemical negativity: an unexpected but intrinsic property of blasts of all phases of chronic myeloid leukemia. Ann Hematol; 2005 Nov;84(12):767-70
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  • [Title] Myeloperoxidase cytochemical negativity: an unexpected but intrinsic property of blasts of all phases of chronic myeloid leukemia.
  • Myeloperoxidase (MPO) cytochemical activity, recognized as a very important hallmark of myeloblasts, is generally negative in chronic myeloid leukemia (CML) blast crisis (BC).
  • Because this finding is unexpected, being not in keeping with the myeloproliferative nature of CML, we tried to ascertain if MPO cytochemical negativity could be an intrinsic property of blasts of CML and hence present in the preblastic phases as well.
  • Myeloperoxidase cytochemistry of peripheral blood blasts in 161 cases of CML, including 103 in chronic phase (CP) and 29 each in accelerated phase (AP) and BC, was assessed and compared with that of 30 cases of acute myeloid leukemia, AML-M2.
  • Blasts of 97 (94.2%) of 103 cases of CP, 28 (96.6%) of 29 cases of AP, and 22 (75.9%) of 29 cases of BC were negative for MPO (<3% MPO-positive blasts).
  • Compared with the strong MPO positivity, both in terms of intensity and proportion, in the AML-M2 cases, the positivity in the CML cases was generally weak and was seen in a small number of blasts (5-15%), except in one case of BC with 20% positive blasts.
  • Absence or, at times, weak MPO cytochemical activity is an intrinsic property of blasts of all phases of CML, and use of the term myeloblast in CML should be understood to refer to a cell with this property.
  • This also explains why MPO cytochemistry, despite its high reputation as a myeloid-lineage marker, generally does not help in CML BC.
  • CML BC should therefore be considered as a possible diagnosis along with acute lymphoblastic leukemia, AML-M0, AML-M7, etc., in the setting of MPO-negative blasts.
  • Similarity between MPO expression pattern in CML, i.e., negative in blasts and positive in the more mature cells, and that during maturation of normal myeloid series of cells shows the deranged myelopoiesis of CML to be undisturbed at least with respect to MPO expression.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Neoplasm Proteins / biosynthesis. Peroxidase / biosynthesis
  • [MeSH-minor] Female. Gene Expression Regulation, Enzymologic. Histocytochemistry. Humans. Leukemia, Myeloid, Acute / enzymology. Leukemia, Myeloid, Acute / pathology. Leukocytes / enzymology. Leukocytes / pathology. Male. Predictive Value of Tests


25. Lahaye T, Riehm B, Berger U, Paschka P, Müller MC, Kreil S, Merx K, Schwindel U, Schoch C, Hehlmann R, Hochhaus A: Response and resistance in 300 patients with BCR-ABL-positive leukemias treated with imatinib in a single center: a 4.5-year follow-up. Cancer; 2005 Apr 15;103(8):1659-69
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  • [Title] Response and resistance in 300 patients with BCR-ABL-positive leukemias treated with imatinib in a single center: a 4.5-year follow-up.
  • BACKGROUND: The advent of imatinib has considerably changed the treatment of chronic myeloid leukemia (CML).
  • Early studies demonstrated high rates of hematologic and cytogenetic responses in all phases of the disease after limited observation periods.
  • METHODS: The authors evaluated long-term outcome, rates of response, and resistance in 300 patients with BCR-ABL-positive leukemias (CML in chronic phase after failure to respond to interferon-alpha [CP], n = 139; accelerated phase [AP], n = 80; myeloid blast crisis [BC], n = 76; lymphoid BC and Philadelphia chromosome-positive acute lymphoblastic leukemia, n = 5) who entered clinical trials with imatinib in a single center after an observation time of 4.5 years.
  • The chance to achieve MCR was higher in patients commencing imatinib earlier in the course of CML.
  • In myeloid BC, the median survival period after the start of imatinib and after diagnosis of BC was 6 and 9 months, respectively.
  • Hematologic resistance occurred in 25%, 41%, and 92% of patients in CP, AP, and myeloid BC, respectively, and was associated with BCR-ABL mutations in 45% of patients and with clonal evolution in 58% of patients.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Fusion Proteins, bcr-abl / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Neoplasm Recurrence, Local / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Benzamides. Blast Crisis. Cytogenetic Analysis. Female. Humans. Imatinib Mesylate. Interferon-alpha / adverse effects. Male. Middle Aged. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction. Salvage Therapy. Survival Rate. Treatment Outcome

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  • [Copyright] (c) 2005 American Cancer Society.
  • (PMID = 15747376.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interferon-alpha; 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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26. 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


27. Schmidt S, Wolf D, Thaler J, Burgstaller S, Linkesch W, Petzer A, Fridrik M, Lang A, Agis H, Valent P, Krieger O, Walder A, Korger M, Schlögl E, Sliwa T, Wöll E, Mitterer M, Eisterer W, Pober M, Gastl G, ASHO CML registry: First annual report of the Austrian CML registry. Wien Klin Wochenschr; 2010 Oct;122(19-20):558-66
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  • [Title] First annual report of the Austrian CML registry.
  • The Austrian chronic myeloid leukemia (CML) registry monitors individual disease courses, treatments applied, clinical outcome, and side effects of CML patients on a nationwide basis to provide data on the "real-life" situation and to complement the information and interpretation gained from the selected patient population observed in clinical trials.
  • This report summarizes the Austrian CML registry data as of March 2009.
  • At diagnosis most patients (n = 163) were in chronic phase (early, late, and secondary), whereas only 4 were in advanced phase.
  • A total of 5 patients progressed from chronic phase to accelerated (n = 3) and blastic phase (n = 2) while receiving imatinib standard dose.
  • Estimated overall survival (OS) rate at 60 months was 90% and progression free survival (PFS) according to European Leukemia Net (ELN) failure definition was 58%.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / mortality. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Registries / statistics & numerical data

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  • (PMID = 20936366.001).
  • [ISSN] 1613-7671
  • [Journal-full-title] Wiener klinische Wochenschrift
  • [ISO-abbreviation] Wien. Klin. Wochenschr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Austria
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28. Jabbour E, Cortes J, Kantarjian H, Giralt S, Andersson BS, Giles F, Shpall E, Kebriaei P, Champlin R, de Lima M: Novel tyrosine kinase inhibitor therapy before allogeneic stem cell transplantation in patients with chronic myeloid leukemia: no evidence for increased transplant-related toxicity. Cancer; 2007 Jul 15;110(2):340-4
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  • [Title] Novel tyrosine kinase inhibitor therapy before allogeneic stem cell transplantation in patients with chronic myeloid leukemia: no evidence for increased transplant-related toxicity.
  • BACKGROUND: Patients undergoing allogeneic hematopoietic stem cell transplantation (HSCT) for chronic myeloid leukemia (CML) are increasingly likely to have received a novel tyrosine kinase inhibitor (NTKI) after failing imatinib mesylate.
  • METHODS: The outcome of 12 patients with CML (1 in chronic phase, 6 in the accelerated phase, and 5 in the blastic phase) who received dasatinib (n = 2), nilotinib (n = 7), or both (n = 3) before HSCT were retrospectively analyzed.
  • Acute and chronic graft-versus-host disease (GVHD) was observed in 7 and 6 patients, respectively.
  • Three patients had disease progression by Day 30 after HSCT.
  • Two patients developed disease recurrence after a median of 12 months.
  • After a median follow-up of 10 months, 7 patients were alive in molecular response and 5 patients had died, 4 of disease progression and 1 of extensive chronic GVHD.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use. Thiazoles / therapeutic use


29. 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


30. Wei Y, Hardling M, Olsson B, Hezaveh R, Ricksten A, Stockelberg D, Wadenvik H: Not all imatinib resistance in CML are BCR-ABL kinase domain mutations. Ann Hematol; 2006 Dec;85(12):841-7
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  • [Title] Not all imatinib resistance in CML are BCR-ABL kinase domain mutations.
  • Point mutations within the ABL kinase domain of the BCR-ABL gene are associated with clinical resistance to imatinib mesylate in chronic myeloid leukemia (CML).
  • To obtain more information about the association between BCR-ABL mutations and type of imatinib resistance, we studied 30 early chronic phase (CP) CML patients, commencing imatinib therapy, using a conventional sequencing technique.
  • Seven patients treated in late CP and three patients treated in the accelerated phase were included for comparison.
  • Likewise, none of 12 early CP patients with detectable BCR-ABL transcripts but in complete hematologic and cytogenetic remission at 12 months displayed any mutation.
  • We conclude that screening early CP patients for BCR-ABL mutations before start of imatinib therapy is not cost-effective.
  • BCR-ABL kinase domain mutations do not appear to explain cytogenetic or molecular (detectable BCR-ABL transcripts by polymerase chain reaction) disease persistence in patients otherwise in stable disease.
  • However, in patients with signs of expanding disease burden, a search for BCR-ABL mutations is warranted.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 17006667.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.- / Protein Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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31. Huang Q: Chronic myelogenous leukemia in accelerated phase. Arch Pathol Lab Med; 2005 May;129(5):710
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic myelogenous 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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32. 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


33. Giles FJ, Abruzzese E, Rosti G, Kim DW, Bhatia R, Bosly A, Goldberg S, Kam GL, Jagasia M, Mendrek W, Fischer T, Facon T, Dünzinger U, Marin D, Mueller MC, Shou Y, Gallagher NJ, Larson RA, Mahon FX, Baccarani M, Cortes J, Kantarjian HM: Nilotinib is active in chronic and accelerated phase chronic myeloid leukemia following failure of imatinib and dasatinib therapy. Leukemia; 2010 Jul;24(7):1299-301
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  • [Title] Nilotinib is active in chronic and accelerated phase chronic myeloid leukemia following failure of imatinib and dasatinib therapy.
  • Nilotinib is a highly selective Bcr-Abl inhibitor approved for imatinib-resistant chronic myeloid leukemia (CML).
  • Nilotinib and dasatinib, a multi-targeted kinase inhibitor also approved for second-line therapy in CML, have different patterns of kinase selectivity, pharmacokinetics, and cell uptake and efflux properties, and thus patients may respond to one following failure of the other.
  • An international phase II study of nilotinib was conducted in CML patients (39 chronic phase (CP), 21 accelerated phase (AP)) after failure of both imatinib and dasatinib.
  • Median times from diagnosis of CP or AP to nilotinib therapy were 89 and 83 months, respectively.
  • Of 17 evaluable patients with CML-AP, 5 (29%) had a confirmed hematological response and 2 (12%) a MCyR.
  • Median overall survival for both populations has not been reached, and the estimated 18-month survival rate in CML-CP was 86% and that at 12 months for CML-AP was 80%.
  • Nilotinib is an effective therapy in CML-CP and -AP following failure of both imatinib and dasatinib therapy.
  • [MeSH-major] Leukemia, Myeloid, Accelerated Phase / drug therapy. Leukemia, Myeloid, Chronic-Phase / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use

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  • (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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34. 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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35. Copelan EA, Crilley PA, Szer J, Dodds AJ, Stevenson D, Phillips G, Elder P, Nivison-Smith I, Avalos BR, Penza S, Topolsky D, Sobecks R, Kalaycio M, Bolwell BJ: Late mortality and relapse following BuCy2 and HLA-identical sibling marrow transplantation for chronic myelogenous leukemia. Biol Blood Marrow Transplant; 2009 Jul;15(7):851-5
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  • [Title] Late mortality and relapse following BuCy2 and HLA-identical sibling marrow transplantation for chronic myelogenous leukemia.
  • Allogeneic hematopoietic stem cell transplantation (HSCT) is the only known curative therapy for chronic myelogenous leukemia (CML).
  • We present mature results in 335 patients with CML who underwent allogeneic bone marrow transplantation (BMT) from HLA-identical siblings following busulfan and cyclophosphamide (BU/Cy2).
  • Two hundred twenty-nine were in chronic phase (CP) and 106 in accelerated or blastic phase at transplantation.
  • The estimated probability of 18-year leukemia-free survival (LFS) for CP patients was 55.6% and for those beyond CP, 10.5%.
  • Of 182 patients who survived leukemia-free at 3 years, the estimated probability of LFS at 18 years was 61.9%.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Bone Marrow Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / mortality. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Siblings
  • [MeSH-minor] Adolescent. Adult. Age Factors. Busulfan / administration & dosage. Cyclophosphamide / administration & dosage. Disease-Free Survival. Female. Follow-Up Studies. Histocompatibility Testing. Humans. Male. Middle Aged. Recurrence. Survival Rate. Transplantation, Homologous

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  • (PMID = 19539217.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 8N3DW7272P / Cyclophosphamide; G1LN9045DK / Busulfan; BUCY-2 protocol
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36. Steinberg M: Dasatinib: a tyrosine kinase inhibitor for the treatment of chronic myelogenous leukemia and philadelphia chromosome-positive acute lymphoblastic leukemia. Clin Ther; 2007 Nov;29(11):2289-308
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  • [Title] Dasatinib: a tyrosine kinase inhibitor for the treatment of chronic myelogenous leukemia and philadelphia chromosome-positive acute lymphoblastic leukemia.
  • The resulting gene product, BCR-ABL, encodes for an abnormal tyrosine kinase (TK) that is a factor in the pathology of chronic myelogenous leukemia (CML).
  • Use of targeted therapy that inhibits BCR-ABL kinase activity may lead to hematologic and cytogenetic responses in affected individuals.
  • The oral TK inhibitor dasatinib was approved in 2006 for use in patients with CML or Philadelphia chromosome-positive acute lymphoblastic leukemia (ALL) who are unable to tolerate or have not responded to other treatments.
  • METHODS: Pertinent information was identified through searches of MEDLINE (1966-May 2007), EMBASE (1980-first quarter 2007), and International Pharmaceutical Abstracts (1970-May 2007) using the terms dasatinib, BMS-354825, chronic myelogenous leukemia, Sprycel, Philadelphia chromosome, and acute lymphoblastic leukemia.
  • RESULTS: Observed mutations in the amino acid sequence of BCR-ABL cause the failure of treatment with existing TK inhibitors.
  • Dasatinib has shown in vitro and in vivo activity against BCR-ABL, including mutations that are resistant to other available TK inhibitors.
  • The 5 phases of START (SRC/ABL Tyrosine kinase inhibition Activity Research Trials of dasatinib) represent the largest and most comprehensive evaluation of dasatinib in the treatment of patients in all stages of CML or Philadelphia chromosome-positive ALL who had undergone previous treatment for leukemia.
  • Dasatanib had the greatest benefit in patients in the chronic phase of CML, with complete hematologic responses in 90% of patients, 52% of whom achieved a major hematologic response.
  • Compared with those in the chronic phase, patients in the accelerated phase or blast crisis of CML, or with Philadelphia chromosome-positive ALL had lower responses.
  • CONCLUSIONS: Dasatinib has a wider spectrum of activity against a broader range of BCR-ABL forms than existing TK inhibitors.
  • It has shown clinical benefit and tolerability in patients in all phases of CML, as well as in those with Philadelphia chromosome-positive ALL.
  • Dasatinib illustrates the potential for targeted drug development based on an understanding of the genetic alterations leading to CML and the development of resistance to treatment.
  • [MeSH-major] Enzyme Inhibitors / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Benzamides. Clinical Trials as Topic. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Dasatinib. Drug Resistance, Neoplasm. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Models, Chemical. Mutation. Piperazines / therapeutic use. Proto-Oncogene Proteins c-bcr / genetics. Randomized Controlled Trials as Topic. Receptors, Purinergic P2 / genetics

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  • [Copyright] Copyright (c) 2007 Excerpta Medica, Inc.
  • (PMID = 18158072.001).
  • [ISSN] 0149-2918
  • [Journal-full-title] Clinical therapeutics
  • [ISO-abbreviation] Clin Ther
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Receptors, Purinergic P2; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr; RBZ1571X5H / Dasatinib
  • [Number-of-references] 52
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37. 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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38. Jabbour E, Kantarjian H, Jones D, Breeden M, Garcia-Manero G, O'Brien S, Ravandi F, Borthakur G, Cortes J: Characteristics and outcomes of patients with chronic myeloid leukemia and T315I mutation following failure of imatinib mesylate therapy. Blood; 2008 Jul 1;112(1):53-5
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  • [Title] Characteristics and outcomes of patients with chronic myeloid leukemia and T315I mutation following failure of imatinib mesylate therapy.
  • Chronic myeloid leukemia (CML) with T315I mutation has been reported to have poor prognosis.
  • At the time of T315I detection, 10 were in chronic phase (CP), 9 in accelerated phase, and 8 in blast phase.
  • Although the T315I mutation is resistant to currently available TKIs, survival of patients with T315I remains mostly dependent on the stage of the disease, with many CP patients having an indolent course.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Point Mutation. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / genetics. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Amino Acid Substitution. Benzamides. Child. Drug Resistance, Neoplasm / genetics. Female. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Male. Middle Aged. Treatment Outcome

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  • (PMID = 18403620.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 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
  • [Other-IDs] NLM/ PMC4081375
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39. Lee TS, Ma W, Zhang X, Giles F, Cortes J, Kantarjian H, Albitar M: BCR-ABL alternative splicing as a common mechanism for imatinib resistance: evidence from molecular dynamics simulations. Mol Cancer Ther; 2008 Dec;7(12):3834-41
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  • [Title] BCR-ABL alternative splicing as a common mechanism for imatinib resistance: evidence from molecular dynamics simulations.
  • Rare cases of chronic myelogenous leukemia (CML) express high levels of alternatively spliced BCR-ABL mRNA with a 35-bp insertion (35INS) between ABL kinase domain exons 8 and 9.
  • This insertion results in a frameshift leading to the addition of 10 residues and truncation of 653 residues due to early termination.
  • Sensitive PCR-based testing showed that 32 of 52 (62%) imatinib-resistant CML patients in chronic phase and 8 of 38 (21%) in accelerated or blast crisis expressed varying levels of the alternatively spliced BCR-ABL mRNA.
  • Simulation results showed that the new residues cause a significant global conformational change, altering imatinib binding in a way similar to that of the T315I mutation and, therefore, providing resistance to imatinib that depends on the level of expression.
  • [MeSH-major] Alternative Splicing. Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm. Fusion Proteins, bcr-abl / physiology. Piperazines / pharmacology. Pyrimidines / pharmacology

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  • [CommentIn] Mol Cancer Ther. 2010 Mar;9(3):772; author reply 772 [20197392.001]
  • [CommentIn] Mol Cancer Ther. 2010 Jul;9(7):2152 [20571070.001]
  • (PMID = 19056677.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
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40. 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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41. D'Antonio J: Chronic myelogenous leukemia. Clin J Oncol Nurs; 2005 Oct;9(5):535-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic myelogenous leukemia.
  • Chronic myelogenous leukemia (CML) represents about 14% of all leukemias and occurs with a frequency of about 1 in 100,000.
  • CML has three phases: the chronic phase, accelerated phase, and blast phase.
  • Most patients are diagnosed during the chronic phase.
  • Ionizing radiation has been implicated in some cases of CML, but in most individuals no cause is known.
  • The Philadelphia chromosome, an acquired genetic mutation represented by a translocation of chromosome 22 and chromosome 9, drives the leukemic changes in CML.
  • Imatinib mesylate, a tyrosine kinase inhibitor, was approved in 2002 for the treatment of all phases of CML.
  • Because of its effectiveness, imatinib has become the treatment of choice for most patients with CML.
  • It is the only curative treatment for CML.
  • Oncology nurses who are knowledgeable about new therapies for CML can be effective resources for their patients.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive
  • [MeSH-minor] Age Distribution. Antineoplastic Agents / therapeutic use. Benzamides. Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 9 / genetics. Dasatinib. Drug Resistance, Neoplasm. Fusion Proteins, bcr-abl / genetics. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Incidence. Leukocyte Count. Mutation / genetics. Nurse's Role. Oncology Nursing. Philadelphia Chromosome. Piperazines / therapeutic use. Polymerase Chain Reaction. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Risk Factors. Stem Cell Transplantation. Thiazoles / therapeutic use. Translocation, Genetic / genetics

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  • [ErratumIn] Clin J Oncol Nurs. 2005 Dec;9(6):672
  • (PMID = 16235580.001).
  • [ISSN] 1092-1095
  • [Journal-full-title] Clinical journal of oncology nursing
  • [ISO-abbreviation] Clin J Oncol Nurs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
  • [Number-of-references] 19
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42. Xiao-Jun H, Lan-Ping X, Kai-Yan L, Dai-Hong L, Huan C, Wei H, Yu-Hong C, Jing-Zhi W, Yao C, Xiao-Hui Z, Hong-Xia S, Dao-Pei L: HLA-mismatched/haploidentical hematopoietic stem cell transplantation without in vitro T cell depletion for chronic myeloid leukemia: improved outcomes in patients in accelerated phase and blast crisis phase. Ann Med; 2008;40(6):444-55
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  • [Title] HLA-mismatched/haploidentical hematopoietic stem cell transplantation without in vitro T cell depletion for chronic myeloid leukemia: improved outcomes in patients in accelerated phase and blast crisis phase.
  • BACKGROUND: Allogeneic hematopoietic stem cell transplantation (allo-HSCT) remains the only proven curative therapy for chronic myeloid leukemia (CML), but lack of human leukocyte antigen (HLA)-matched sibling or unrelated donors has restricted its application.
  • AIM: To evaluate the outcomes of CML patients who underwent haploidentical allo-HSCT.
  • RESULTS: Our data showed that the cumulative incidence of acute graft-versus-host disease (GVHD) was 64.52%, and grade III-IV was 26.45%, 61.79% had chronic GVHD, and 28.93% had extensive chronic GVHD.
  • Probability of 1-year and 4-year leukemia-free survival was similar in chronic phase (CP) 1, CP2/CR2, accelerated phase, and blast crisis patients.
  • Probability of 4-year overall survival varied as 76.5% (CP1), 85.7% (CP2/CR2), 73.3% (accelerated phase), and 61.5% (blast crisis).
  • Multivariate analysis indicated that factors affecting transplantation outcomes were HLA-B+DR mismatches versus others for II-III acute GVHD and III-IV acute GVHD, the stage of disease at transplantation for relapse, and the time from diagnosis to transplantation for leukemia-free survival, overall survival, and transplantation-related mortality.
  • In our protocol, survival of HSCT for advanced CML was similar to stable stage.
  • [MeSH-major] Blast Crisis / therapy. Hematopoietic Stem Cell Transplantation / methods. Histocompatibility Testing. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Directed Tissue Donation. Female. Graft Survival. Graft vs Host Disease. Humans. Male. Middle Aged. Opportunistic Infections. Survival Analysis. Transplantation Conditioning. Transplantation, Homologous. Young Adult


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


44. Qian J, Wang YL, Lin J, Yao DM, Xu WR, Wu CY: Aberrant methylation of the death-associated protein kinase 1 (DAPK1) CpG island in chronic myeloid leukemia. Eur J Haematol; 2009 Feb;82(2):119-23
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  • [Title] Aberrant methylation of the death-associated protein kinase 1 (DAPK1) CpG island in chronic myeloid leukemia.
  • The epigenetic changes of TSGs are now recognized as a mechanism contributing to the development of chronic myeloid leukemia (CML).
  • To clarify the role of DAPK1 in CML, we examined the methylation status of DAPK1 in 49 patients with CML using methylation-specific polymerase chain reaction.
  • The aberrant methylation of the DAPK1 gene was found in 25 of 49 (51.0%) CML cases, not in all controls.
  • No correlation was found between DAPK1 gene methylation and the age, hematologic parameters, chromosomal abnormalities, the types and levels of bcr/abl transcripts of CML patients.
  • However, correlation could be observed between the sex and the status of DAPK1 methylation in CML patients (R = 0.374, P = 0.008).
  • Furthermore, there was a significant correlation between DAPK1 methylation and the stages of CML (R = 0.354, P = 0.013).
  • The CML patients in accelerated phase (AP) and blast crisis (BC) had higher frequency of DAPK1 methylation than those in chronic phase (CP) (75.0% vs. 34.5%) (chi(2) = 7.776, P = 0.005).
  • In one patient, the status of DAPK1 methylation became positive on the transition from CP to AP and BC.
  • These results suggested that DAPK1 promoter methylation might play a significant role in the progression of CML.
  • [MeSH-major] Apoptosis Regulatory Proteins / genetics. Calcium-Calmodulin-Dependent Protein Kinases / genetics. CpG Islands. DNA Methylation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics


45. Almeida A, Castro I, Coutinho J, Guerra L, Marques H, Pereira AM: [Recommendations for diagnosis, treatment and monitoring of chronic myeloid leukemia]. Acta Med Port; 2009 Sep-Oct;22(5):537-44
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  • [Title] [Recommendations for diagnosis, treatment and monitoring of chronic myeloid leukemia].
  • [Transliterated title] Recomendações para o diagnóstico, tratamento e monitorização da leucemia mielóide crónica.
  • Chronic Myeloid Leukemia (CML) is a clonal stem cell disease characterized by the expression of the fusion protein bcr-abl1, which has deregulated tirosine-kinase activity.
  • Tyrosine kinase inhibitors (TKIs), and in particular imatinib, introduced fundamental changes in the treatment of CML, becoming, in most cases, the first-line treatment of choice in the chronic phase of this disease.
  • Compared to other available therapies imatinib results in a marked increase in overall survival, tolerability and quality of life.
  • The introduction of second generation TKI, with increased potency against bcr-abl1, expanded the number of therapeutic options for this disease and offers an alternative for patients resistant or intolerant to imatinib or who have progressed to the accelerated phase under this therapy.
  • In order to achieve optimal outcomes, TKI therapy must be managed rigorously, requiring a careful monitoring of treatment response in pre-established time periods, thus permitting disease evaluation and safe decision of the most adequate option.
  • The objective of this paper is to review the criteria for CML diagnosis, treatment and monitoring, with recommendations as to the most adequate therapeutic choice according to the response to TKI therapy.
  • The paper also focuses the current lines of investigation and debate areas that in the short term can significantly change the therapeutic scenario in this disease.
  • These recommendations, supported by published scientific evidence and by the clinical practice of the expert panel involved in their elaboration, may constitute an important instrument for a better understanding and standardisation of the treatment and monitoring of CML in Portugal.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy


46. Mahon FX, Molimard M: Correlation between trough imatinib plasma concentration and clinical response in chronic myeloid leukemia. Leuk Res; 2009 Aug;33(8):1147-8; author reply 1149-50
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  • [Title] Correlation between trough imatinib plasma concentration and clinical response in chronic myeloid leukemia.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / pharmacokinetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / administration & dosage. Piperazines / pharmacokinetics. Pyrimidines / administration & dosage. Pyrimidines / pharmacokinetics
  • [MeSH-minor] Benzamides. Cytogenetic Analysis. Drug Monitoring. Female. Fusion Proteins, bcr-abl / analysis. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Leukemia, Myeloid, Accelerated Phase. Leukemia, Myeloid, Chronic-Phase. Male. Middle Aged. Polymerase Chain Reaction. Risk Assessment

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  • [CommentOn] Leuk Res. 2009 Feb;33(2):271-5 [18762338.001]
  • (PMID = 19395027.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comment; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [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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47. 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
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  • [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


48. Nicolini FE, Mauro MJ, Martinelli G, Kim DW, Soverini S, Müller MC, Hochhaus A, Cortes J, Chuah C, Dufva IH, Apperley JF, Yagasaki F, Pearson JD, Peter S, Sanz Rodriguez C, Preudhomme C, Giles F, Goldman JM, Zhou W: Epidemiologic study on survival of chronic myeloid leukemia and Ph(+) acute lymphoblastic leukemia patients with BCR-ABL T315I mutation. Blood; 2009 Dec 17;114(26):5271-8
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  • [Title] Epidemiologic study on survival of chronic myeloid leukemia and Ph(+) acute lymphoblastic leukemia patients with BCR-ABL T315I mutation.
  • The BCR-ABL T315I mutation represents a major mechanism of resistance to tyrosine kinase inhibitors (TKIs).
  • The objectives of this retrospective observational study were to estimate overall and progression-free survival for chronic myeloid leukemia in chronic-phase (CP), accelerated-phase (AP), or blastic-phase (BP) and Philadelphia chromosome-positive (Ph)(+) acute lymphoblastic leukemia (ALL) patients with T315I mutation.
  • These results confirm that survival of patients harboring a T315I mutation is dependent on disease phase at the time of mutation detection.
  • [MeSH-major] Genes, abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Disease-Free Survival. Drug Resistance, Neoplasm / genetics. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Mutation. Retrospective Studies. Young Adult


49. Shah NP: Dasatinib. Drugs Today (Barc); 2007 Jan;43(1):5-12
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  • Preclinical studies have shown dasatinib to be a much more potent inhibitor of BCR-ABL than imatinib is, and to harbor efficacy against nearly all imatinib-resistant BCR-ABL mutants.
  • Phase I clinical studies have been conducted in imatinib-resistant and -intolerant chronic myeloid leukemia and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia.
  • Multinational phase II studies have confirmed the phase I experience and have led to accelerated approval by the U.S.
  • Food and Drug Administration for the treatment of imatinib-resistant and -intolerant chronic myeloid leukemia as well as its full approval for the treatment of therapy-resistant Ph+ acute lymphoblastic leukemia.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / pharmacology. Pyrimidines / therapeutic use. Thiazoles / pharmacology. Thiazoles / therapeutic use
  • [MeSH-minor] Dasatinib. Drug Evaluation, Preclinical. Fusion Proteins, bcr-abl. Humans. Protein-Tyrosine Kinases / antagonists & inhibitors

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  • [Copyright] c 2007 Prous Science. All rights reserved.
  • (PMID = 17315048.001).
  • [ISSN] 1699-3993
  • [Journal-full-title] Drugs of today (Barcelona, Spain : 1998)
  • [ISO-abbreviation] Drugs Today
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [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
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50. 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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51. 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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52. Phan CL, Megat Baharuddin PJ, Chin LP, Zakaria Z, Yegappan S, Sathar J, Tan SM, Purushothaman V, Chang KM: Amplification of BCR-ABL and t(3;21) in a patient with blast crisis of chronic myelogenous leukemia. Cancer Genet Cytogenet; 2008 Jan 1;180(1):60-4
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  • [Title] Amplification of BCR-ABL and t(3;21) in a patient with blast crisis of chronic myelogenous leukemia.
  • The Philadelphia (Ph) chromosome, or t(9;22), is the hallmark of chronic myelogenous leukemia (CML).
  • It results in juxtaposition of the 5' part of the BCR gene on chromosome 22 to the 3' part of the ABL1 gene (previously ABL) on chromosome 9.
  • CML is clinically characterized by three distinct phases: chronic, accelerated, and blast phase.
  • Blast crisis is characterized by the rapid expansion of a population of differentiation arrested blast cells (myeloid or lymphoid cells population), with secondary chromosomal abnormalities present.
  • We report a case of myeloid blast crisis of CML resistant to imatinib mesylate and chemotherapy.
  • By use of cytogenetic, fluorescence in situ hybridization, and comparative genomic hybridization methods, we identified a cluster of BCR-ABL amplification on inverted duplication of the Ph chromosome with t(3;21)(q26;q22) and increased genomic levels of the RUNX1 gene (previously AML1).
  • The t(3;21)(q26;q22) is a recurrent chromosomal abnormality in some cases of CML blast phase and in treatment-related myelodysplastic syndrome and acute myeloid leukemia.
  • Amplification or copy number increase of RUNX1 has been reported in childhood acute lymphoblastic leukemia.
  • Our study indicated that the progenitor of CML was BCR-ABL dependent through the amplification of Ph chromosome as a mechanism of resistance to imatinib therapy.
  • The coexistence of BCR-ABL and t(3;21)(q26;q22) with RUNX1 rearrangement might play a pivotal role in the CML blast transformation.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 3. Fusion Proteins, bcr-abl / genetics. Gene Amplification. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Translocation, Genetic

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  • (PMID = 18068536.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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53. 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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54. Tian J, Cheng H, Xu KL, Pan XY: [Detection of phosphotyrosine in chronic myeloid leukemia cells with PY20 antibody and its clinical applications]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Aug;17(4):1056-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Detection of phosphotyrosine in chronic myeloid leukemia cells with PY20 antibody and its clinical applications].
  • The objective of this study was to investigate the specificity of detecting the phosphotyrosine level with anti-phosphotyrosine monoclonal antibody PY20 for diagnosis and prognosis of patients with chronic myeloid leukemia (CML) and the possibility of its clinical application.
  • The positive rate of PY20 in 28 newly diagnosed CML patients was detected by flow cytometry using anti-PY20 antibody, the bcr-abl fusion gene was detected by nested RT-PCR, the Ph chromosome was measured by R-banding cytogenetic analysis, and the coincidence of PY20 positive rate with results of bcr-abl fusion gene and Ph chromosome detection was compared.
  • In addition, the positive rate of PY20, the changes of bcr-abl fusion gene and Ph chromosome were determined in follow up 7 CML patients after allo-hematopoietic stem cell transplantation.
  • The results indicated that the positive rates of PY20 in 28 newly diagnosed CML patients in groups of chronic phase (CP), accelerated phase (AP), and blast phase (BP) were (40.31% +/- 1.22)%, (77.28 +/- 1.14)% and (78.12 +/- 1.32)% respectively.
  • The positive rate of PY20 in CP was lower than that in AP and BP (p < 0.05).
  • There was no difference in positive rate of PY20 between AP and BP (p > 0.05).
  • The positive rates of PY20 in patients with CR, PR and NR were (15.56% +/- 1.51)%, (38.73% +/- 2.31)% and (60.43% +/- 2.04)% respectively.
  • The positive and negative coincidence between PY20 and RT-PCR was 92.31% and 95.45% respectively.
  • The positive and negative coincidence between PY20 and Ph Chromosome in newly diagnosed patients was 88.46% and 95.46% respectively.
  • Ph chromosome and PY20 were all negative in 7 CML patients after allo-HSCT.
  • Bcr-abl fusion gene was negative persistently in 5 patients, but in the other 2 patients, the fusion gene was persistently positive.
  • In conclusion, the detection of the level of phosphotyrosine in CML cells has high sensitivity and specificity.
  • The results of PY20 cell positive rate combined with detection of bcr/abl fusion gene and Ph chromosome might be useful in diagnosis as a good index of monitoring.


55. Sanz J, Montesinos P, Saavedra S, Lorenzo I, Senent L, Planelles D, Larrea L, Martín G, Palau J, Jarque I, Martínez J, de la Rubia J, Moscardó F, Martinez D, Gómez I, López M, Sanz MA, Sanz GF: Single-unit umbilical cord blood transplantation from unrelated donors in adult patients with chronic myelogenous leukemia. Biol Blood Marrow Transplant; 2010 Nov;16(11):1589-95
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  • [Title] Single-unit umbilical cord blood transplantation from unrelated donors in adult patients with chronic myelogenous leukemia.
  • Clinical studies focused on outcomes of umbilical cord blood transplantation (UCBT) for patients with chronic myelogenous leukemia (CML) in need of allogeneic stem cell transplantation and lacking an HLA-matched adult donor are limited.
  • We analyzed the outcome of 26 adults with CML receiving single-unit UCBT from unrelated donors after myeloablative conditioning at a single institution.
  • At the time of transplantation, 7 patients (27%) were in first chronic phase (CP), 11 (42%) were in second CP, 2 (8%) were in accelerated phase (AP), and 6 (23%) were in blast crisis (BC).
  • The cumulative incidence (CI) of myeloid engraftment was 88% at a median time of 22 days and was significantly better for patients receiving higher doses of CD34(+) cells.
  • The CI of acute graft-versus-host disease (GVHD) grade II-IV was 61%, that of acute GVHD grade III-IV was 39%, and that of chronic extensive GVHD was 60%.
  • After a median follow-up of 8 years, none of the patients relapsed, giving an overall disease-free survival (DFS) at 8 years of 41%.
  • These results demonstrate that UCBT from unrelated donors can be a curative treatment for a substantial number of patients with CML.
  • [MeSH-major] Blood Donors. Cord Blood Stem Cell Transplantation / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy
  • [MeSH-minor] Adolescent. Adult. Cause of Death. Disease-Free Survival. Female. Graft Rejection / epidemiology. Graft Survival. Graft vs Host Disease / diagnosis. Graft vs Host Disease / epidemiology. Histocompatibility. Humans. Leukocyte Count. Male. Middle Aged. Neutrophils / cytology. Platelet Count. Recurrence. Retrospective Studies. Transplantation Chimera. Treatment Outcome. Young Adult

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  • [Copyright] Copyright © 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20553927.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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56. 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


57. Li RJ, Zhang GS, Chen YH, Zhu JF, Lu QJ, Gong FJ, Kuang WY: Down-regulation of mitochondrial ATPase by hypermethylation mechanism in chronic myeloid leukemia is associated with multidrug resistance. Ann Oncol; 2010 Jul;21(7):1506-14
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  • [Title] Down-regulation of mitochondrial ATPase by hypermethylation mechanism in chronic myeloid leukemia is associated with multidrug resistance.
  • BACKGROUND: To identify novel proteins involved in multidrug resistance in chronic myeloid leukemia (CML).
  • The promoter hypermethylation in mitochondrial ATPase was found to be attributed to the adriamycin-resistant phenotype of both K562/A02 (methylated frequency 18.18%) and CML primary cells in accelerated phase (methylated frequency 7.95%) or blast crisis (methylated frequency 26.59%).
  • CONCLUSION: Down-regulation of mitochondrial ATPase can lead to adriamycin resistance in CML and the mechanism is associated with DNA methylation regulation.

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  • (PMID = 20038517.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / P-Glycoprotein; 0 / RNA, Messenger; 3X2S926L3Z / trichostatin A; 80168379AG / Doxorubicin; EC 3.6.3.- / ATP5I protein, human; EC 3.6.3.- / Mitochondrial Proton-Translocating ATPases; M801H13NRU / Azacitidine
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58. Luo Y, Pan J, Shi JM: [Clinical observation of Gleevec combined with myeloablative allogeneic stem cells transplantation in treatment of chronic myeloid leukemia]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2007 Jul;36(4):343-7
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  • [Title] [Clinical observation of Gleevec combined with myeloablative allogeneic stem cells transplantation in treatment of chronic myeloid leukemia].
  • OBJECTIVE: To observe the efficacy of Gleevec combined with myeloablative allogeneic stem cells transplantation(Allo-SCT) for the treatment of chronic myeloid leukemia (CML).
  • METHODS: Nine patients with CML were treated with Gleevec before and after Allo-SCT, with 5 in the chronic phase (CP), 2 in the accelerated phase (AP) and 2 in the blast-crisis phase (BP).
  • Three cases suffered from acute GVHD and 4 from chronic GVHD.
  • The rate of disease free survival was 88.9% after a median follow-up of 31 m (range 7 approximately 34 m).
  • CONCLUSION: The treatment of CML consisting of myeloablative Allo-SCT combined with Gleevec before and after transplantation is an effective and safe method for CML.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Peripheral Blood Stem Cell Transplantation. Piperazines / therapeutic use. Pyrimidines / therapeutic use


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

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  • [Copyright] Copyright 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20005967.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases
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60. Jiang Q, Chen SS, Jiang B, Jiang H, Lu Y, Qiu JY, Lu DP: [Clonal evolution of abnormal Philadelphia chromosome-negative cells after imatinib mesylate therapy in patients with Philadelphia chromosome-positive chronic myelogenous leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2005 Jan;26(1):23-6
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  • [Title] [Clonal evolution of abnormal Philadelphia chromosome-negative cells after imatinib mesylate therapy in patients with Philadelphia chromosome-positive chronic myelogenous leukemia].
  • OBJECTIVE: To investigate clonal evolution of abnormal Philadelphia chromosome-negative cells (Ph- CE) after imatinib mesylate therapy in patients with Philadelphia chromosome-positive chronic myelogenous leukemia (Ph+ CML).
  • METHODS: Bone marrow cells G-banding karyotype was evaluated every 3 months in 100 patients with Ph+ CML after achieving hematologic responses on the course of imatinib therapy.
  • There were 54 patients in chronic phase (CP), 37 in accelerated phase (AP) and 9 in blast phase (BP).
  • CONCLUSION: Ph- CE occurred in about 11% of the patients with Ph+ CML who achieved major or minor cytogenetic responses on imatinib therapy.
  • After a median follow-up of more than 2 years, most of the patients with Ph- CE were in a stable status with no disease progression.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / drug therapy. Philadelphia Chromosome. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 15946504.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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61. Ocheni S, Iwanski GB, Schafhausen P, Zander AR, Ayuk F, Klyuchnikov E, Zabelina T, Fiedler W, Schnittger S, Hochhaus A, Brümmendorf TH, Kröger N, Bacher U: Characterisation of extramedullary relapse in patients with chronic myeloid leukemia in advanced disease after allogeneic stem cell transplantation. Leuk Lymphoma; 2009 Apr;50(4):551-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterisation of extramedullary relapse in patients with chronic myeloid leukemia in advanced disease after allogeneic stem cell transplantation.
  • Recently, higher extramedullary relapse rates following allogeneic stem cell transplantation (SCT) in myeloid malignancies were reported e.g. because of selection of poor-risk patients.
  • We analysed five consecutive patients with post-transplant extramedullary relapse of chronic myeloid leukemia (CML) out of a total of 24 patients (21%) undergoing allo-SCT.
  • All five patients with extramedullary relapse had clonal evolution and a history of blast phase (BP).
  • In particular, 56% of the patients in BP had extramedullary relapse with no extramedullary relapse in patients with chronic/accelerated phase.
  • Research should focus on prospective studies aiming to improve treatment of extramedullary relapse in stem cell recipients with CML with a special focus on the role of second generation tyrosine kinase inhibitors.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Stem Cell Transplantation / methods


62. 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
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  • [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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63. Dutcher JP, Morris EL, Gaynor B, Paietta E, Wiernik PH: A pilot study of carboplatin and mitoxantrone in blast crisis of chronic myeloid leukemia. Med Oncol; 2010 Sep;27(3):728-35
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  • [Title] A pilot study of carboplatin and mitoxantrone in blast crisis of chronic myeloid leukemia.
  • The efficacy and toxicity of carboplatin plus mitoxantrone in blast crisis of chronic myeloid leukemia (CMLBC) were evaluated.
  • Median time from diagnosis of CML to BC was 4.25 years (range 0-11 years).
  • CMLBC was myeloid in 13 patients, lymphoid in six, and megakaryocytic in one.
  • All patients were Philadelphia (Ph) chromosome positive; four had a single Ph chromosome, five had double Ph chromosome, three had abnormalities of chromosome 17, and eight had complex cytogenetic abnormalities.
  • Prior treatment for chronic phase included hydroxyurea (12 patients), interferon-alpha (11 patients), cytarabine or all-trans retinoic acid, three patients each and other agents (four patients).
  • Eight patients (five myeloid and three lymphoid) had an objective response (median duration, 3 months).
  • Five had complete responses (CR) of 2, 3, 3, 6, and 6+ months duration, and three had partial responses (PR) for 1, 2, and 4 months.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blast Crisis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • [MeSH-minor] Adult. Aged. Carboplatin / administration & dosage. Carboplatin / adverse effects. Female. Follow-Up Studies. Humans. Leukemia, Myeloid, Accelerated Phase / drug therapy. Male. Middle Aged. Mitoxantrone / administration & dosage. Mitoxantrone / adverse effects. Pancytopenia / chemically induced. Pilot Projects. Remission Induction. Survival Analysis. Treatment Outcome


64. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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65. Velev N, Cortes J, Champlin R, Jones D, Rondon G, Giralt S, Borthakur G, Kantarjian HM, De Lima M: Stem cell transplantation for patients with chronic myeloid leukemia resistant to tyrosine kinase inhibitors with BCR-ABL kinase domain mutation T315I. Cancer; 2010 Aug 1;116(15):3631-7
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  • [Title] Stem cell transplantation for patients with chronic myeloid leukemia resistant to tyrosine kinase inhibitors with BCR-ABL kinase domain mutation T315I.
  • Although many imatinib-resistant mutations respond well to second-generation TKIs, the threonine-to-isoleucine mutation at codon 315 of the breakpoint cluster region/v-abl Abelson murine leukemia viral oncogene protein fusion Bcr-Abl (T315I) is insensitive to all currently available TKIs.
  • METHODS: Eight patients with TKI-resistant CML who had T315I mutations underwent 9 transplantations.
  • At the time of SCT, 2 patients were in chronic phase, 3 patients were in accelerated phase; and 3 patients were in second chronic phase.
  • The best outcome was for patients who underwent transplantation in chronic phase, and both of those patients remained alive and in complete molecular remission 14 months and 42 months after SCT.
  • CONCLUSIONS: The current results indicated that SCT is an effective strategy for patients with CML who have the T315I mutation, particularly in earlier stages.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Mutation. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Stem Cell Transplantation


66. Suttorp M, Claviez A, Bader P, Peters C, Gadner H, Ebell W, Dilloo D, Kremens B, Kabisch H, Führer M, Zintl F, Göbel U, Klingebiel T: Allogeneic stem cell transplantation for pediatric and adolescent patients with CML: results from the prospective trial CML-paed I. Klin Padiatr; 2009 Nov-Dec;221(6):351-7
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  • [Title] Allogeneic stem cell transplantation for pediatric and adolescent patients with CML: results from the prospective trial CML-paed I.
  • PURPOSE: Stem cell transplantation (SCT) can definitely cure chronic myeloid leukemia (CML), a rare disease in childhood.
  • We prospectively evaluated the results of early SCT in pediatric CML after standardized pretreatment with hydroxyurea+/-interferon.
  • PATIENTS AND METHODS: Between 1995 and 2004, 200 children (median age: 12.4 years) were enrolled and stratified: given the availability of an HLA-matched related donor (MRD), SCT was scheduled within 6 months and otherwise from an unrelated donor (UD) within 12 months following diagnosis.
  • RESULTS: 176 patients underwent SCT; from MRD within median 4 months and from UD within median 11 months after diagnosis.
  • At SCT, 158 patients were in chronic phase (CP1 or CP2), 9 patients were in accelerated phase and 9 patients were in blast crisis (BC).
  • A trend for better OS in CP1 was observed if SCT was performed within 6 months (n=49; 74+/-9%), compared to 7-12 months (n=52; 62+/-15%), and >12 months (n=43; 62+/-17%) after diagnosis, respectively (p=0.157).
  • Transplant-related mortality and graft-versus-host disease mainly contributed to the inferior outcome in UD and HLA-mismatched SCT.
  • CONCLUSION: These data from the first prospective trial on CML restricted to children and adolescents might be considered for decision making when balancing the risks of SCT against the increasing use of imatinib as upfront treatment for CML.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy
  • [MeSH-minor] Adolescent. Antineoplastic Agents / therapeutic use. Benzamides. Bone Marrow Purging. Child. Disease-Free Survival. Female. Graft vs Host Disease / mortality. Humans. Imatinib Mesylate. Kaplan-Meier Estimate. Male. Piperazines / therapeutic use. Prospective Studies. Pyrimidines / therapeutic use. Transplantation Conditioning / methods. Transplantation, Homologous

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  • [Copyright] Georg Thieme Verlag KG Stuttgart.New York.
  • (PMID = 19890786.001).
  • [ISSN] 1439-3824
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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67. Galimberti S, Cervetti G, Guerrini F, Testi R, Pacini S, Fazzi R, Simi P, Petrini M: Quantitative molecular monitoring of BCR-ABL and MDR1 transcripts in patients with chronic myeloid leukemia during Imatinib treatment. Cancer Genet Cytogenet; 2005 Oct 1;162(1):57-62
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  • [Title] Quantitative molecular monitoring of BCR-ABL and MDR1 transcripts in patients with chronic myeloid leukemia during Imatinib treatment.
  • In search for a possible correlation, BCR-ABL and MDR1 expression were measured in 115 serial bone marrow samples from 33 CML patients during Imatinib treatment.
  • All patients achieved complete hematologic responses, and 22 patients also achieved complete cytogenetic responses, with median BCR-ABL mRNA values significantly lower than those observed in the group of cases that were persistently Philadelphia positive.
  • All three cases treated during the accelerated phase showed disease progression after an initial period of remission; all presented either increased levels of BCR-ABL or MDR1 3 months before clinical progression.
  • In the subgroup of cases treated during the chronic phase, BCR-ABL and MDR1 levels were significantly correlated after 3 and 6 months (88 and 80%, respectively) but not after 12 months of treatment (32%).
  • Reported data maintain that MDR1 expression would play an important role in Imatinib resistance when the disease is not fully controlled (e.g., progressive disease or during the first months of treatment).
  • [MeSH-major] Fusion Proteins, bcr-abl / metabolism. Genes, MDR. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use


68. Buesche G, Ganser A, Schlegelberger B, von Neuhoff N, Gadzicki D, Hecker H, Bock O, Frye B, Kreipe H: Marrow fibrosis and its relevance during imatinib treatment of chronic myeloid leukemia. Leukemia; 2007 Dec;21(12):2420-7
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  • [Title] Marrow fibrosis and its relevance during imatinib treatment of chronic myeloid leukemia.
  • In chronic myeloid leukemia (CML), imatinib may reverse bone marrow fibrosis (MF).
  • Fifty-nine patients with Ph+ CML treated with > or = 400 mg imatinib/day were examined for MF in 6- to 12-month intervals.
  • Evolutions of FFI and MF were independent significant predictors of imatinib failure (P=0.0031), accelerated phase and death of patients (P=0.0001; multivariate analyses).
  • Imatinib effectively reverses initial MF in CML, but neither eliminates its unfavorable prognosis nor guarantees completely against new evolution of MF.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Primary Myelofibrosis / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Benzamides. Biomarkers, Tumor / analysis. Bone Marrow / drug effects. Bone Marrow / pathology. Disease Progression. Follow-Up Studies. Fusion Proteins, bcr-abl / analysis. Humans. Imatinib Mesylate. Interferon-alpha / therapeutic use. Janus Kinase 2 / genetics. Male. Middle Aged. Pilot Projects. Prognosis. Recurrence. Remission Induction. Salvage Therapy

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  • (PMID = 17805334.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Biomarkers, Tumor; 0 / Interferon-alpha; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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69. Radich JP, Dai H, Mao M, Oehler V, Schelter J, Druker B, Sawyers C, Shah N, Stock W, Willman CL, Friend S, Linsley PS: Gene expression changes associated with progression and response in chronic myeloid leukemia. Proc Natl Acad Sci U S A; 2006 Feb 21;103(8):2794-9
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  • [Title] Gene expression changes associated with progression and response in chronic myeloid leukemia.
  • Chronic myeloid leukemia (CML) is a hematopoietic stem cell disease with distinct biological and clinical features.
  • The biologic basis of the stereotypical progression from chronic phase through accelerated phase to blast crisis is poorly understood.
  • We used DNA microarrays to compare gene expression in 91 cases of CML in chronic (42 cases), accelerated (17 cases), and blast phases (32 cases).
  • Three thousand genes were found to be significantly (P < 10(-10)) associated with phase of disease.
  • A comparison of the gene signatures of chronic, accelerated, and blast phases suggest that the progression of chronic phase CML to advanced phase (accelerated and blast crisis) CML is a two-step rather than a three-step process, with new gene expression changes occurring early in accelerated phase before the accumulation of increased numbers of leukemia blast cells.
  • Studies of CML patients who relapsed after initially successful treatment with imatinib demonstrated a gene expression pattern closely related to advanced phase disease.

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  • (PMID = 16477019.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE4170
  • [Grant] United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / CA-18029; United States / NCI NIH HHS / CA / CA-85053
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / DNA-Binding Proteins; 0 / Kruppel-Like Transcription Factors; 0 / MZF1 protein, human; 0 / Peptide Elongation Factor 1; 0 / Piperazines; 0 / Pyrimidines; 0 / Transcription Factors; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC1413797
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70. Moen MD, McKeage K, Plosker GL, Siddiqui MA: Imatinib: a review of its use in chronic myeloid leukaemia. Drugs; 2007;67(2):299-320
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  • [Title] Imatinib: a review of its use in chronic myeloid leukaemia.
  • Imatinib (Gleevec, Glivec) is a synthetic tyrosine kinase inhibitor used in the treatment of chronic myeloid leukaemia (CML).
  • It is specifically designed to inhibit the breakpoint cluster region (BCR)-Abelson (ABL) fusion protein that results from the chromosomal abnormality known as the Philadelphia chromosome.
  • CML is characterised by this abnormality, which leads to abnormalities of the peripheral blood and bone marrow including an increase in the number of granular leukocytes.
  • Imatinib is approved in numerous countries worldwide for the treatment of newly diagnosed Philadelphia chromosome-positive (Ph+) chronic-phase CML, Ph+ accelerated-phase or blast-crisis CML, and in patients with Ph+ chronic-phase CML who have failed to respond to interferon-alpha therapy.
  • It is also indicated in paediatric patients with newly diagnosed Ph+ chronic-phase CML, in accelerated-phase or blast-crisis CML, or in chronic-phase CML after failure of interferon-alpha therapy or when the disease has recurred after haematopoietic stem cell transplantation (HSCT).
  • Imatinib is effective and generally well tolerated in patients with Ph+ CML.
  • In patients with newly diagnosed chronic-phase CML, imatinib was more effective than interferon-alpha plus cytarabine in preventing progression of the disease and in achieving haematological and cytogenetic responses.
  • Patients with accelerated-phase or blast-crisis CML, or those who have not responded to prior interferon-alpha therapy also benefit from imatinib treatment.
  • The introduction of imatinib has had a marked impact on outcomes in patients with CML.
  • It remains a valuable treatment for all stages of the disease, especially initial treatment of newly diagnosed Ph+ chronic-phase CML, and is endorsed by European and US treatment guidelines as a first-line option.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 17284091.001).
  • [ISSN] 0012-6667
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 90
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71. Kim TD, Türkmen S, Schwarz M, Koca G, Nogai H, Bommer C, Dörken B, Daniel P, le Coutre P: Impact of additional chromosomal aberrations and BCR-ABL kinase domain mutations on the response to nilotinib in Philadelphia chromosome-positive chronic myeloid leukemia. Haematologica; 2010 Apr;95(4):582-8
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  • [Title] Impact of additional chromosomal aberrations and BCR-ABL kinase domain mutations on the response to nilotinib in Philadelphia chromosome-positive chronic myeloid leukemia.
  • BACKGROUND: Additional chromosomal aberrations in Philadelphia chromosome-positive chronic myeloid leukemia are non-random and strongly associated with disease progression, but their prognostic impact and effect on treatment response is not clear.
  • Point mutations in the BCR-ABL kinase domain are probably the most common mechanisms of imatinib resistance.
  • DESIGN AND METHODS: We assessed the influence of additional chromosomal aberrations and BCR-ABL kinase domain mutations on the response to the second-generation tyrosine kinase inhibitor nilotinib after imatinib-failure.
  • Standard cytogenetic analysis of metaphases was performed to detect additional chromosomal aberrations and the BCR-ABL kinase domain was sequenced to detect point mutations.
  • RESULTS: Among 53 patients with a median follow-up of 16 months, of whom 38, 5 and 10 were in chronic phase, accelerated phase and blast crisis, respectively, 19 (36%) had additional chromosomal aberrations and 20 (38%) had BCR-ABL kinase domain mutations.
  • Among patients with chronic phase disease, overall survival at 2 years was 100% and 62% for patients without or with additional chromosomal aberrations, respectively (P=0.0024).
  • BCR-ABL kinase domain mutations were associated with lower remission rates in response to nilotinib, with 9 of 20 (45%) of these patients achieving a major cytogenetic remission as compared to 26 of 33 (79%) patients without mutations (P<0.05).
  • However, overall survival was not affected by BCR-ABL kinase domain mutations.
  • CONCLUSIONS: Whereas BCR-ABL kinase domain mutations may confer more specific resistance to nilotinib, which will predominantly affect response rates, the presence of additional chromosomal aberrations may reflect genetic instability and, therefore, intrinsic aggressiveness of the disease which will be less amenable to subsequent alternative treatments and thus negatively affect overall survival.
  • Conventional cytogenetic analyses remain mandatory during follow-up of patients with chronic myeloid leukemia under tyrosine kinase inhibitor therapy.
  • [MeSH-major] Chromosome Aberrations. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Philadelphia Chromosome. Point Mutation / genetics. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Benzamides. Clinical Trials as Topic. Disease Progression. Drug Resistance, Neoplasm. Female. Follow-Up Studies. Gene Expression Regulation, Leukemic. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction. Salvage Therapy. Survival Rate. Treatment Outcome


72. Shen Q, Zhou JW, Zhu GR, Yang YY, Qiu HR, Zhu GR, Xia W, Jiang PJ: [Chronic myeloid leukemia onset with marked thrombocythemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Apr;14(2):247-51
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  • [Title] [Chronic myeloid leukemia onset with marked thrombocythemia].
  • This study was aimed to investigate the clinical, pathological and biological features of a special case of chronic myeloid leukemia (CML) with marked thrombocythemic onset.
  • The morphological changes of cells were analyzed by using bone marrow smear and biopsy; Ph chromosome, a specific marker of CML, was assayed by conventional chromosomal analysis and fluorescence in situ hybridization, bcr/abl fusion gene was detected by reverse transcription-polymerase chain reaction.
  • The results indicated that CML mimicked essential thrombocythemia (ET) at presentation was relatively rare and might be misdiagnosed as ET, bone marrow smear and biopsy revealed, marked thrombocytosis and moderate leukocytosis; RT-PCR, FISH and conventional chromosomal analysis demonstrated the existence of Ph chromosome and bcr/abl fusion gene.
  • This special CML could progress into accelerated phase or blast crisis.
  • Patients diagnosed as Ph+ ET might progress into CML and showed a high tendency to myelofibrosis and blastic transformation.
  • It is concluded that the value of routine cytogenetical and molecular biological analysis in diagnosis for potential CML cases, which mimicked ET as in this presentation, is very distinctive, and the importance is magnified by the recent availability of imatinib, a specific inhibitor of the bcr/abl tyrosine kinase produced by the Philadelphia chromosome.
  • Every case of "ET" should be tested for the Philadelphia chromosome and bcr/abl transcript.


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

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  • [Copyright] Copyright (c) 2009 S. Karger AG, Basel.
  • (PMID = 19887785.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Benzamides; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / GFI1 protein, human; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Transcription Factors; 8A1O1M485B / Imatinib Mesylate
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75. 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


76. Guilhot F, Druker B, Larson RA, Gathmann I, So C, Waltzman R, O'Brien SG: High rates of durable response are achieved with imatinib after treatment with interferon alpha plus cytarabine: results from the International Randomized Study of Interferon and STI571 (IRIS) trial. Haematologica; 2009 Dec;94(12):1669-75
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  • BACKGROUND: Imatinib is the standard of care for newly diagnosed chronic-phase chronic myeloid leukemia.
  • DESIGN AND METHODS: Patients were allowed to cross over to the opposite treatment for intolerance, lack of response, disease progression, and, following release of the initial efficacy data, reluctance to remain on therapy with interferon-alpha plus cytarabine.
  • Estimated rates of freedom from progression to accelerated or blast phase and overall survival were 91% and 89%, respectively, at 48 months after starting imatinib.
  • CONCLUSIONS: This is the largest analysis to date describing the efficacy of imatinib in patients who have received prior therapies for chronic myeloid leukemia and it demonstrates excellent responses to this treatment. (ClinicalTrials.gov identifier: NCT00006343).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy

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  • (PMID = 19648168.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00006343
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Pyrimidines; 04079A1RDZ / Cytarabine; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC2791923
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77. 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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78. Boma PO, Durosinmi MA, Adediran IA, Akinola NO, Salawu L: Clinical and prognostic features of Nigerians with chronic myeloid leukemia. Niger Postgrad Med J; 2006 Mar;13(1):47-52
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  • [Title] Clinical and prognostic features of Nigerians with chronic myeloid leukemia.
  • AIMS AND OBJECTIVES: Chronic myeloid leukemia (CML).
  • PATIENTS AND METHODS: CML patients confirmed at the OAUTHC, Ile-Ife between June 1986 and December 1999 were studied prospectively until death or the last visit to the clinic.
  • Stages of the disease at diagnosis, presenting clinical features and laboratory parameters, as well as the drug history were noted for each patient.
  • Survival of each patient was computed from the date of diagnosis until the date of death.
  • Philadelphia chromosome was positive in the five patients (12.0%) that underwent cytogenetic analysis.
  • Thirty-three of the patients (78.6%) presented in treatable chronic phase and the other 9 (21.4%) were seen in advanced stages (7 in accelerated & 2 in blastic phase).
  • The median survival of patients that presented in chronic phase was 31.7 months compared to 0.16 months in patients presenting in advanced stages, the difference was statistically significant (log rank=7.8, p-value=0.005).
  • Significant positive correlation was obtained between spleen size and total white cell count at diagnosis (r=0.36, p=0.02).
  • Univariate regression analysis showed negative relationship between survival and ages of patients at diagnosis, haematocrit value, spleen and liver sizes, and blast count.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology


79. Giles FJ, Rosti G, Beris P, Clark RE, le Coutre P, Mahon FX, Steegmann JL, Valent P, Saglio G: Nilotinib is superior to imatinib as first-line therapy of chronic myeloid leukemia: the ENESTnd study. Expert Rev Hematol; 2010 Dec;3(6):665-73
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  • [Title] Nilotinib is superior to imatinib as first-line therapy of chronic myeloid leukemia: the ENESTnd study.
  • Nilotinib (Tasigna(®)) is a more potent BCR-ABL inhibitor than imatinib and was designed to overcome imatinib's deficiencies.
  • Nilotinib has significant efficacy in patients with chronic myeloid leukemia (CML) in chronic phase, accelerated phase and blastic phase, following imatinib failure.
  • Based on the results of the Evaluating Nilotinib Efficacy and Safety in Clinical Trials-Newly Diagnosed Patients (ENESTnd) study, the US FDA has granted accelerated approval of nilotinib for the treatment of adult patients with newly diagnosed Philadelphia chromosome-positive CML in chronic phase.
  • Nilotinib, a designer agent built on the imatinib scaffold, has proven superior to its template agent by every significant surrogate marker we use in monitoring CML.
  • Nilotinib's clinical superiority over imatinib, as demonstrated by the ENESTnd study, has established it as an agent that we believe is a significant further step towards the cure of CML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use


80. Zonder JA, Schiffer CA: Update on practical aspects of the treatment of chronic myeloid leukemia with imatinib mesylate. Curr Hematol Malig Rep; 2006 Sep;1(3):141-51
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  • [Title] Update on practical aspects of the treatment of chronic myeloid leukemia with imatinib mesylate.
  • Imatinib (imatinib mesylate, Gleevec(R) [formerly known as STI571], Novartis Pharmaceuticals, Basel, Switzerland) is a protein tyrosine kinase inhibitor that is approved by the US Food and Drug Administration for patients with all phases of chronic myeloid leukemia (CML).
  • Imatinib is remarkably effective as treatment for CML in the chronic phase (at a dosage of 400 mg/d) and the accelerated phase (at 600 mg/d).
  • At this time, it remains to be seen whether the chronic phase of CML can be extended sufficiently in some patients so that they are functionally "cured," and also whether the increased rate of major molecular response induced by doses of imatinib higher than 400 mg/d will further improve overall survival of patients with CML in the chronic phase.
  • The value of molecular monitoring of response in patients with CML in the chronic phase is examined.
  • Although imatinib 800 mg/d can induce dramatic responses in patients with myeloid blast crisis, lymphoid blast crisis, and Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL), the responses are usually incomplete and of short duration.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Fusion Proteins, bcr-abl / antagonists & inhibitors. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 20425345.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
  • [Number-of-references] 68
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81. Deremer DL, Ustun C, Natarajan K: Nilotinib: a second-generation tyrosine kinase inhibitor for the treatment of chronic myelogenous leukemia. Clin Ther; 2008 Nov;30(11):1956-75
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  • [Title] Nilotinib: a second-generation tyrosine kinase inhibitor for the treatment of chronic myelogenous leukemia.
  • BACKGROUND: Nilotinib, a second-generation tyrosine kinase inhibitor (TKI) formerly known as AMN107, was approved by the US Food and Drug Administration (FDA) on October 29, 2007, for the treatment of adult patients with chronic-phase (CP) and accelerated-phase (AP) Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML) resistant to or intolerant of prior treatment that included imatinib.
  • OBJECTIVE: The purpose of this review was to evaluate the pharmacology, pharmacokinetic properties, and pharmacodynamic properties of nilotinib; results of clinical trials in patients with CML, Ph+ acute lymphoblastic leukemia (ALL), and gastrointestinal stromal tumors (GISTs); and potential drug interactions.
  • Search terms included, but were not limited to, nilotinib, AMN107, chronic myelogenous leukemia, acute lymphoblastic leukemia, bcr-abl, imatinib resistance, adverse events, pharmacology, and clinical trials.
  • RESULTS: Nilotinib is an orally bioavailable derivative of imatinib with improved specificity toward the breakpoint cluster region-Abelson murine leukemia (bcr-abl) viral protooncogene.
  • In preclinical studies, nilotinib was found to have activity against 32 of 33 imatinib-resistant bcr-abl mutations, but not against the T3151 mutation.
  • In 2 Phase II, open-label, single-arm clinical studies, nilotinib was found to be beneficial in patients with CML that was imatinib resistant or intolerant.
  • Overall, 58% of patients with CML-CP achieved a major cytogenetic response; 42%, a complete cytogenetic response; and 77%, a complete hematologic response (CHR).
  • Of patients whose disease had progressed to AP, nilotinib was associated with major cytogenetic response in 32%; complete cytogenetic response in 19%; and CHR in 30%.
  • At 12 months, an estimated 56% of patients lacked progression of disease, and the estimated overall survival rate was 82%.
  • CONCLUSIONS: Nilotinib is an oral second-generation bcr-abl TKI indicated for the treatment of imatinib resistant or -intolerant Ph+ CML-CP and -AP in adults.
  • Positive clinical activity and tolerability have been reported in clinical trials.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
  • [MeSH-minor] Animals. Clinical Trials as Topic. Fusion Proteins, bcr-abl. Gastrointestinal Stromal Tumors / drug therapy. Humans. Models, Biological. Molecular Structure. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


82. 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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83. Wu LL, Zeng QS, Yang MZ, Miao HW, Xia RX, Wang L, Ni J: [Detection of ABL kinase domain point mutations in chronic myeloid leukemia patients receiving imatinib treatment]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Feb;18(1):49-53
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  • [Title] [Detection of ABL kinase domain point mutations in chronic myeloid leukemia patients receiving imatinib treatment].
  • This study was purposed to evaluate ABL tyrosine kinase point mutations in imatinib-treated chronic myeloid leukemia (CML) patients and their clinical significance.
  • 51 bone marrow samples from 28 imatinib-resistant patients and 10 newly diagnosed CML patients were collected.
  • ABL kinase domain of bcr-abl allele was amplified by nested reverse transcription-polymerase chain reaction, followed by purifying, directly sequencing and sequence homology analysis of amplified products in order to determine the existence and type of point mutation.
  • The results showed that the point mutations were found in 12 of 38 patients, and all the 12 ones progressed to advanced disease or death.
  • The incidence of the point mutation was 17.6%, 45.5% and 44.4% in chronic, accelerated and blast phase respectively.

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  • (PMID = 20137117.001).
  • [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 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
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84. Mughal TI, Goldman JM: Chronic myeloid leukemia: why does it evolve from chronic phase to blast transformation? Front Biosci; 2006;11:198-208
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  • [Title] Chronic myeloid leukemia: why does it evolve from chronic phase to blast transformation?
  • Clinically chronic myeloid leukemia is a biphasic or triphasic disease that is usually diagnosed in the initial 'chronic', 'indolent' or 'stable' phase and then spontaneously evolves after some years into an advanced phase.
  • This advanced phase can sometimes be subdivided into an earlier accelerated phase and a later blast phase or blast transformation--in about one-half of patients the chronic phase transforms unpredictably and abruptly to a blast phase, while in the other half of patients, the disease evolves somewhat more gradually, through an accelerated phase, which may last for months or years, before a blast phase ensues; this may have myeloblastic or lymphoblastic features.
  • Although much is now known about the molecular biology of the disease, the molecular basis of disease progression is still obscure.
  • The popular thinking has been that one or more probably a sequence of additional genetic events occurs in the BCR-ABL positive clone.
  • Here we review what is known of the mechanisms underlying the evolution of chronic myeloid leukemia from a chronic phase to a blast transformation.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Lymphocyte Activation
  • [MeSH-minor] Animals. Apoptosis. Biological Evolution. Blast Crisis. Cytogenetics. Cytokinesis. DNA Repair. Disease Progression. Fusion Proteins, bcr-abl / chemistry. Humans. Janus Kinase 1. Lymphocytes / metabolism. Models, Biological. Mutation. Philadelphia Chromosome. Phosphatidylinositol 3-Kinases / metabolism. Proteasome Endopeptidase Complex / metabolism. Protein Structure, Tertiary. Protein-Tyrosine Kinases / metabolism. Proto-Oncogene Proteins c-myc / metabolism. RNA, Messenger / metabolism. Recombinant Fusion Proteins / metabolism. STAT5 Transcription Factor / metabolism. Time Factors

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  • (PMID = 16146725.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; 0 / Recombinant Fusion Proteins; 0 / STAT5 Transcription Factor; EC 2.7.010.2 / JAK1 protein, human; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / Janus Kinase 1; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Number-of-references] 95
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85. Popova EY, Claxton DF, Lukasova E, Bird PI, Grigoryev SA: Epigenetic heterochromatin markers distinguish terminally differentiated leukocytes from incompletely differentiated leukemia cells in human blood. Exp Hematol; 2006 Apr;34(4):453-62
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  • [Title] Epigenetic heterochromatin markers distinguish terminally differentiated leukocytes from incompletely differentiated leukemia cells in human blood.
  • In order to identify the chromatin regulatory factors associated with incomplete cell differentiation and impaired chromatin condensation in hematological malignancies, we examined expression levels of major heterochromatin proteins in normal blood cells and cells derived from a number of chronic and acute myeloid leukemia patients exhibiting different degrees of differentiation.
  • RESULTS: While the major epigenetic heterochromatin factor, histone H3 methylated at lysine 9, is present in all cell types, its main counterparts, nonhistone proteins, heterochromatin proteins 1 (HP1) alpha, beta, and gamma, are dramatically reduced in peripheral blood leukocytes of normal donors and chronic myeloid leukemia patients, but are substantially increased in the blood of accelerated phase and blast crisis patients.
  • HP1 and MNEI levels inversely correlate in a number of normal and leukemia myeloid cells and show strikingly opposite coordinated changes during differentiation of U937 cell line induced by retinoic acid.
  • CONCLUSIONS: Our results suggest that repression of HP1 and accumulation of MNEI are linked to terminal cell differentiation and that their levels may be monitored in blood cell populations to detect transitions in cell differentiation associated with leukemia progression and treatment.
  • [MeSH-major] Cell Differentiation. Epigenesis, Genetic. Heterochromatin / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukocytes / metabolism

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  • (PMID = 16569592.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM-59118
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Chromosomal Proteins, Non-Histone; 0 / Heterochromatin; 0 / Histones; 0 / Neoplasm Proteins; 0 / Proteins; 0 / Serpins; 147416-07-7 / SERPINB1 protein, human; 5688UTC01R / Tretinoin
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86. 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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87. Imataki O, Shintani T, Waki F, Ohnishi H, Ishida T: [Tolerability of imatinib for patients with chronic myelogeneous leukemia (CML)]. Gan To Kagaku Ryoho; 2008 Nov;35(11):1863-7
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  • [Title] [Tolerability of imatinib for patients with chronic myelogeneous leukemia (CML)].
  • We reviewed a patients' cohort treated with imatinib in our hospital in 2007 for chronic myelogeneous leukemia (CML).
  • The disease status at onset was chronic phase in 13 patients and accelerated phase in 1.
  • In 4 of these 6 intolerant cases, CR was maintained 2 years after the start of imatinib therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Tolerance. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Benzamides. Disease Progression. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Stem Cell Transplantation. Survival Rate. Young Adult

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  • (PMID = 19011333.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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88. Koh Y, Kim I, Yoon SS, Kim BK, Kim DY, Lee JH, Lee KH, Park E, Kim HJ, Sohn SK, Joo YD, Kim SJ, Chung J, Shin HJ, Kim SH, Kim CS, Song HS, Kim MK, Hyun MS, Ahn JS, Jung CW, Park S, Korean Society of Hematology CML working party: Phase IV study evaluating efficacy of escalated dose of imatinib in chronic myeloid leukemia patients showing suboptimal response to standard dose imatinib. Ann Hematol; 2010 Jul;89(7):725-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase IV study evaluating efficacy of escalated dose of imatinib in chronic myeloid leukemia patients showing suboptimal response to standard dose imatinib.
  • The aim of this phase IV study was to (1) to define efficacy of escalating dose imatinib in chronic myeloid leukemia (CML) patients showing suboptimal response to standard dose imatinib and (2) to find markers that predict the response to escalating doses of imatinib.
  • CML patients in chronic phase (CP) who failed to achieve optimal response with 400 mg/day imatinib or patients in accelerated phase (AP) or blast crisis (BC) who failed to achieve complete hematologic response after 3 months of 400-600 mg/day imatinib were enrolled.
  • Patients received imatinib for at least 12 months or until the disease progression or intolerable toxicity.
  • Along with cytogenetic response (CyR), molecular response was assessed with BCR-ABL/ABL ratio.
  • Baseline BCR-ABL gene mutation test was performed.
  • TTFx was longer in patients who achieved greater than 50% reduction in BCR-ABL/ABL within 6 months (early molecular responder (EMR)) compared with those who did not (non-EMR; p < 0.001).
  • In conclusion, escalated dose imatinib shows considerable efficacy with tolerable toxicity in CML patients showing suboptimal response to standard dose imatinib.
  • EMR is an early predictive marker for positive imatinib response.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Blast Crisis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Adolescent. Adult. Aged. Benzamides. Biomarkers, Tumor / metabolism. Disease-Free Survival. Female. Fusion Proteins, bcr-abl / genetics. Fusion Proteins, bcr-abl / metabolism. Humans. Imatinib Mesylate. Male. Middle Aged. Mutation. Survival Rate

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  • (PMID = 20179930.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase IV; Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Biomarkers, Tumor; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Investigator] Pak S; Kim I; Yoon SS; Kim HJ; Sohn SK; Chung J; Shin HJ; Kim CS; Kim MK; Jung CW; Kim BS; Kim YK; Kim JS; Kim JS; Kwak JY; Lee NR; Min YH; Park CW; Suk JO; Lee JH; Zang DY; Cheong JW; Jo DY; Kim BS; Kim SH; Ryu HM; Nam SH; Moon YC; Park KT; Park MR; Park E; Park JH; Park CH; Bang SM; Bae SH; Lee MH; Jang SS; Jang JH; Chung CH; Chi HS; Choi SI; Lee JL
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89. Jakubowska J, Czyz M: [Novel inhibitors of Bcr-Abl]. Postepy Hig Med Dosw (Online); 2006;60:697-706
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  • [Title] [Novel inhibitors of Bcr-Abl].
  • [Transliterated title] Alternatywne dla STI571 inhibitory kinazy Bcr-Abl.
  • STI571 (imatinib; Gleevec) was developed to specifically target the tyrosine kinase activity of the Bcr-Abl protein in Philadelphia chromosome-positive chronic myeloid leukemia (CML).
  • It is the first-line drug for newly diagnosed CML, with remarkable efficacy to patients in the chronic phase of this cancer.
  • However, CML patients in the accelerated phase or blast crisis often relapse due to drug resistance.
  • STI571 fails to eradicate leukemic stem cells, and BCR-ABL(+).
  • The necessity for alternative or additional treatment for STI571-resistant leukemia resulted in the development of a second generation of drugs for targeted therapies.
  • In this review a literature overview of the alternative inhibitors which were designed to override STI571 resistance and decrease the aberrant kinase activity of Bcr-Abl protein with higher efficiency is presented.

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  • (PMID = 17245319.001).
  • [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 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / AP23464; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Hydroxamic Acids; 0 / Indoles; 0 / PD 166326; 0 / PD 180970; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 0 / Pyridones; 0 / Pyrimidines; 0 / Thiazoles; 859212-16-1 / bafetinib; 8A1O1M485B / Imatinib Mesylate; 8L70Q75FXE / Adenosine Triphosphate; 9647FM7Y3Z / panobinostat; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
  • [Number-of-references] 53
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90. Tam CS, Kantarjian H, Garcia-Manero G, Borthakur G, O'Brien S, Ravandi F, Shan J, Cortes J: Failure to achieve a major cytogenetic response by 12 months defines inadequate response in patients receiving nilotinib or dasatinib as second or subsequent line therapy for chronic myeloid leukemia. Blood; 2008 Aug 1;112(3):516-8
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  • [Title] Failure to achieve a major cytogenetic response by 12 months defines inadequate response in patients receiving nilotinib or dasatinib as second or subsequent line therapy for chronic myeloid leukemia.
  • Projected 1-year progression to hematologic failure, accelerated phase, or blast phase was also significantly different (3% vs 17%, P = .003).
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Pyrimidines / administration & dosage. Thiazoles / administration & dosage

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  • [Cites] Blood. 2001 Nov 15;98(10):3074-81 [11698293.001]
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  • (PMID = 18492956.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ PMC4082324
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91. Yeh CH, Tseng R, Zhang Z, Cortes J, O'Brien S, Giles F, Hannah A, Estrov Z, Keating M, Kantarjian H, Albitar M: Circulating heat shock protein 70 and progression in patients with chronic myeloid leukemia. Leuk Res; 2009 Feb;33(2):212-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Circulating heat shock protein 70 and progression in patients with chronic myeloid leukemia.
  • We evaluated the association of circulating levels of heat shock protein 70 (Hsp70) in plasma with clinical behavior and progression in 139 chronic myeloid leukemia (CML) patients.
  • Circulating Hsp70 levels did not differ significantly between CML patients in the chronic phase (n=93; median 33.24 ng/mL, range 3.89-128.2 ng/mL) and those in the accelerated/blast phase (n=46; median 26.57 ng/mL, range 4.5-114.7 ng/mL).
  • However, overall CML patients had significantly higher levels of Hsp70 than healthy subjects (n=95, median 4.17 ng/mL, range 1.75-24.7 ng/mL) (P<0.001).
  • In chronic phase CML patients, Hsp70 levels above the median were associated with a higher rate of progression to the accelerated/blast phase and a tendency toward shorter survival.
  • Plasma Hsp70 thus could be a potential marker for predicting disease progression in patients with chronic phase CML.
  • [MeSH-major] HSP70 Heat-Shock Proteins / blood. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Benzamides. Biomarkers / blood. Disease Progression. Humans. Imatinib Mesylate. Leukemia, Myeloid, Accelerated Phase / diagnosis. Leukemia, Myeloid, Chronic-Phase / diagnosis. Middle Aged. Piperazines / therapeutic use. Prognosis. Pyrimidines / therapeutic use. Young Adult

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  • [CommentIn] Leuk Res. 2009 Feb;33(2):205-6 [18752847.001]
  • (PMID = 18715642.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Biomarkers; 0 / HSP70 Heat-Shock Proteins; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ NIHMS593155; NLM/ PMC4163801
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92. Zhara M, Mourad H, Farouk G, Elbatch M, Ezzat S, Sami W: Molecular detection of survivin expression, antiapoptotic gene, and other prognostic markers, how they are correlated and how it could be of prognostic value in chronic myeloid leukemia patient. Egypt J Immunol; 2007;14(2):51-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular detection of survivin expression, antiapoptotic gene, and other prognostic markers, how they are correlated and how it could be of prognostic value in chronic myeloid leukemia patient.
  • Chronic myeloid leukemia (CML) is a malignant disease of heampoitic stem cell resulting from clonal expansion of leukemic myeloid cells.
  • The aim of the work is to analyze the expression of survivin in CML patient in chronic, accelerated and blastic phases and its correlation with other prognostic markers.
  • The study included 50 CML patients (24 females and 26 males) and 10 healthy individuals (4 female and 6 male) as a control group.
  • The studied groups were classified into group (I), 10 healthy individuals as a control group, group (II), 20 CML patients in chronic phase, Group (III), 15 CML patients in accelerated phase and Group (IV), 15 CML patients in blastic phase.
  • The accelerated and blastic phases of the disease showed the highest significance (p < 0.001) than the chronic phase.
  • Serum markers; survivin, IL6 and beta2M showed significant increase in the blastic phase, accelerated phase and chronic phase (p < 0.001, p < 0.001 and p < 0.001) respectively.
  • A significant positive correlation was found between level of survivin expression and the other prognostic markers; high leucocytic count (r = 0.52), high peripheral basophile count (r= 0.81) and high peripheral blast cell count (r = 0.66), high level of serum survivin (r = 0.87), beta2 M (r = 0.76) and IL-6 (r= 0.90).
  • In conclusion, survivin is expressed in most cases of CML patients and its over expression is associated with bad prognosis.


93. Lindauer M, Hochhaus A: Dasatinib. Recent Results Cancer Res; 2010;184:83-102
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It potently inhibits BCR-ABL and SRC-family kinases (SRC, LCK, YES, FYN), but also c-KIT, PDGFR-alpha and beta, and ephrin receptor kinase.Dasatinib is about 300 times more potent than imatinib in cells expressing unmutated BCR-ABL in vitro.
  • The drug has demonstrated activity against clinically relevant mutations, including those associated with poor prognosis during ongoing imatinib therapy.Dasatinib is approved for the treatment of patients with BCR-ABL-positive chronic myeloid leukemia (CML), resistant or intolerant to imatinib in chronic, accelerated, and blast phase.
  • It also is approved for the treatment of Philadelphia Chromosome positive (Ph+) acute lymphoblastic leukemia (ALL) resistant or intolerant to imatinib.A single daily dose of 100 mg in chronic phase CML results in high hematologic and molecular remission rates and prolongation of survival.
  • In accelerated and blastic phase as well as in ALL, 70 mg twice daily is recommended.
  • Complete hematologic and cytogenetic remissions (CR) frequently occur even in this patient group with poor prognosis.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use

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  • (PMID = 20072833.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Oncogene Proteins v-abl; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.2 / src-Family Kinases; RBZ1571X5H / Dasatinib
  • [Number-of-references] 68
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94. Ridruejo E, Cacchione R, Villamil AG, Marciano S, Gadano AC, Mandó OG: Imatinib-induced fatal acute liver failure. World J Gastroenterol; 2007 Dec 28;13(48):6608-111
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Imatinib mesylate is a drug that has been approved for treatment of chronic myeloid leukemia (CML) in blast crisis, accelerated or chronic phase, and also for advanced gastrointestinal stromal tumors.
  • She was diagnosed with CML and began treatment with imatinib mesylate at a dose of 400 mg/d.
  • [MeSH-minor] Acetaminophen / adverse effects. Acetaminophen / therapeutic use. Analgesics, Non-Narcotic / adverse effects. Analgesics, Non-Narcotic / therapeutic use. Benzamides. Fatal Outcome. Female. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Middle Aged. Pain / drug therapy