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1. Oshimi K: Progress in understanding and managing natural killer-cell malignancies. Br J Haematol; 2007 Nov;139(4):532-44
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  • The World Health Organization classification of haematolymphoid tumours recognizes three categories of natural killer (NK)-cell neoplasms: blastic NK-cell lymphoma, aggressive NK-cell leukaemia, and extranodal NK/T-cell lymphoma, nasal-type.
  • Myeloid/NK-cell precursor acute leukaemia may also develop from precursor NK cells.
  • Aggressive NK-cell leukaemia is rare and has a poor prognosis.
  • [MeSH-major] Killer Cells, Natural / pathology. Leukemia, Lymphoid / therapy
  • [MeSH-minor] Acute Disease. Cell Lineage. Cell Transformation, Neoplastic / pathology. Chronic Disease. Humans. Neoplasm Staging. Preleukemia / pathology. Prognosis

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  • (PMID = 17916099.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 132
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2. Swords R, Quinn J, Fay M, O'Donnell R, Goldman J, Murphy PT: CML clonal evolution with resistance to single agent imatinib therapy. Clin Lab Haematol; 2005 Oct;27(5):347-9
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  • [Title] CML clonal evolution with resistance to single agent imatinib therapy.
  • We describe a 58-year-old male diagnosed with chronic myeloid leukaemia (CML) who failed to have a cytogenetic response to interferon-alpha and hydroxyurea.
  • On subsequent therapy with imatinib mesylate he failed to have any cytogenetic response but also developed a complex clonal evolution with an additional Philadelphia (Ph) chromosome and trisomy 8 respectively in two Ph-positive subclones.
  • The case demonstrates the efficacy of combined treatment with imatinib and cytarabine in the management of CML resistant to single agent imatinib.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Transformation, Neoplastic / chemically induced. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / adverse effects. Pyrimidines / adverse effects
  • [MeSH-minor] Benzamides. Clone Cells / pathology. Cytarabine / therapeutic use. Drug Resistance, Neoplasm. Humans. Hydroxyurea / therapeutic use. Imatinib Mesylate. Interferon-alpha / therapeutic use. Male. Middle Aged. Philadelphia Chromosome. Remission Induction / methods. Treatment Failure. Trisomy

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  • (PMID = 16178920.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Pyrimidines; 04079A1RDZ / Cytarabine; 8A1O1M485B / Imatinib Mesylate; X6Q56QN5QC / Hydroxyurea
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3. De Moerloose B, Muylaert A, Gemmel F, Janssens A, Poppe B, Dhooge C, Benoit Y, Van Hove W, Philippé J: Repetitive analyses of P-glycoprotein in chronic myeloid leukaemia. Acta Clin Belg; 2000 Jul-Aug;55(4):215-21
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  • [Title] Repetitive analyses of P-glycoprotein in chronic myeloid leukaemia.
  • P-glycoprotein, a pump located in the plasma cell membrane, extrudes several clinically important drugs from the cell, and hence causes multidrug resistance.
  • Reversing clinical drug resistance is possible by using agents that inhibit the activity of P-glycoprotein.
  • We describe the results of sequential flow cytometric determinations of P-glycoprotein expression and activity in two patients suffering from acute lymphoblastic transformation of chronic myeloid leukaemia.
  • However, after chemotherapy containing P-glycoprotein substrates, a significant expression was found in both patients and the functional flow cytometric test was positive.
  • In order to achieve an accurate selection of patients that might benefit from the clinical use of P-gp inhibitors, repeated analyses are indicated in each patient suffering from acute leukaemia, during the course of the illness.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. P-Glycoprotein / antagonists & inhibitors
  • [MeSH-minor] Child. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Female. Flow Cytometry. Follow-Up Studies. Gene Expression Regulation, Neoplastic. Humans. Immunophenotyping. Male. Middle Aged. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 11036680.001).
  • [ISSN] 1784-3286
  • [Journal-full-title] Acta clinica Belgica
  • [ISO-abbreviation] Acta Clin Belg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] BELGIUM
  • [Chemical-registry-number] 0 / P-Glycoprotein
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4. Drummond MW, Holyoake TL: Tyrosine kinase inhibitors in the treatment of chronic myeloid leukaemia: so far so good? Blood Rev; 2001 Jun;15(2):85-95
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  • [Title] Tyrosine kinase inhibitors in the treatment of chronic myeloid leukaemia: so far so good?
  • Chronic myeloid leukaemia (CML) is characterized by marked expansion of the myeloid series, and is thought to arise as a direct result of the bcr-abl fusion-gene.
  • It has been shown that the increased tyrosine kinase activity of BCR-ABL is a requirement for transformation and is, therefore, a legitimate target for pharmacological inhibition.
  • Recent laboratory evidence, however, suggests that the development of drug resistance is a possibility (via amplification of the bcr-abl fusion gene, overexpression of P-glycoprotein or binding of ST1571 to alpha1 acid glycoprotein) and that combination therapy including ST1571 should be considered.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Benzamides. Enzyme Inhibitors / therapeutic use. Fusion Proteins, bcr-abl / antagonists & inhibitors. Humans. Imatinib Mesylate. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • [Copyright] Copyright 2001 Harcourt Publishers Ltd.
  • (PMID = 11409908.001).
  • [ISSN] 0268-960X
  • [Journal-full-title] Blood reviews
  • [ISO-abbreviation] Blood Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 126
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5. Edlin R, Connock M, Tubeuf S, Round J, Fry-Smith A, Hyde C, Greenheld W: Azacitidine for the treatment of myelodysplastic syndrome, chronic myelomonocytic leukaemia and acute myeloid leukaemia. Health Technol Assess; 2010 May;14 Suppl 1:69-74
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  • [Title] Azacitidine for the treatment of myelodysplastic syndrome, chronic myelomonocytic leukaemia and acute myeloid leukaemia.
  • This paper presents a summary of the evidence review group (ERG) report into the clinical effectiveness and cost-effectiveness of azacitidine (aza) compared with conventional care regimes (CCR) for higher risk patients with myelodysplastic syndrome (MDS), chronic myelomonocytic leukaemia (CMML) and acute myeloid leukaemia (AML), based on the evidence submission from the manufacturer to the National Institute for Health and Clinical Excellence (NICE) as part of the single technology appraisal process.
  • The patient outcomes governing relative effectiveness and cost-effectiveness were defined as overall survival, time to progression (TTP) to AML, adverse events and health-related quality of life (HRQoL).
  • The results showed that: the median overall survival was 24.5 months on aza, compared with 15.0 months in the CCR group (p = 0.0001); the response rates were low (complete remission 17% aza versus 8% CCR); the median time to transformation to AML was greater in the aza group (17.8 versus 11.5 months; p < 0.0001); and of patients who were red blood cell (RBC) transfusion-dependent at baseline, 45% of those on aza became RBC transfusion-independent during the treatment period, compared with 11.8% in the CCR group (p < 0.0001).
  • Using the issues identified in the earlier analysis, the ERG conducted those repairs to the revised model that were feasible within time constraints.
  • The results of these exploratory analyses indicated that: for standard-dose chemotherapy (SDC)-treated patients, of six treatment options available, best supportive care (BSC) was likely the most cost-effective option up to a threshold of 51,000 pounds/quality-adjusted life-year (QALY) [beyond 51,000 pounds/QALY, aza + low-dose chemotherapy (LDC) became cost-effective]; for LDC-treated patients, of four options available, BSC was again the most cost-effective option up to a willingness-to-pay threshold of 51,000 pounds/QALY (aza + LDC became cost-effective after 51,000 pounds/QALY); for BSC-treated patients, aza + BSC became cost-effective relative to BSC at a threshold of about 52,000 pounds/QALY.
  • At the time of writing, the guidance appraisal consultation document issued by NICE on 4 March 2010 states that azacitidine is not recommended as a treatment option for people not eligible for haemopoietic stem cell transplantation with the the following conditions: intermediate-2 and high-risk MDS according to the International Prognostic Scoring System, CMML with 10-29% marrow blasts without myeloproliferative disorder, or with AML with 20-30% blasts and multilineage dysplasia, according to World Health Organization classification.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myelomonocytic, Chronic / drug therapy. Myelodysplastic Syndromes / drug therapy


6. Aichberger KJ, Herndlhofer S, Agis H, Sperr WR, Esterbauer H, Rabitsch W, Knöbl P, Haas OA, Thalhammer R, Schwarzinger I, Sillaber C, Jäger U, Valent P: Liposomal cytarabine for treatment of myeloid central nervous system relapse in chronic myeloid leukaemia occurring during imatinib therapy. Eur J Clin Invest; 2007 Oct;37(10):808-13
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  • [Title] Liposomal cytarabine for treatment of myeloid central nervous system relapse in chronic myeloid leukaemia occurring during imatinib therapy.
  • BACKGROUND: Central nervous system (CNS) relapse in chronic myeloid leukaemia (CML) is rare and if recorded is usually found to occur in patients with lymphoblastic transformation.
  • PATIENTS AND METHODS: We report on two CML patients who developed a myeloid CNS relapse during treatment with imatinib.
  • One patient was in major cytogenetic response at the time of CNS relapse.
  • In both cases, the myeloid origin of neoplastic cells in the cerebrospinal fluid (CSF) was demonstrable by immunophenotyping, and their leukaemic origin by detection of the BCR/ABL oncoprotein.
  • In one patient, additional CNS radiation was performed, whereas in the other, consecutive treatment with dasatinib (70 mg per os twice daily) was started.
  • RESULTS: In response to therapy, the clinical symptoms resolved, and the leukaemic cells in the CSF disappeared in both cases.
  • CONCLUSIONS: 'Anatomic' resistance against imatinib in the CNS can lead to a myeloid CNS relapse.
  • Liposomal cytarabine with or without radiation is effective as local therapy in these patients.
  • For systemic treatment and prophylaxis, BCR/ABL kinase inhibitors crossing the blood-brain barrier such as dasatinib should be considered in patients with CNS relapse.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Central Nervous System Neoplasms / drug therapy. Cytarabine / administration & dosage. Cytarabine / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / therapeutic use
  • [MeSH-minor] Aged. Benzamides. Dasatinib. Drug Therapy, Combination. Female. Humans. Imatinib Mesylate. Liposomes. Male. Middle Aged. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use. Treatment Outcome

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  • (PMID = 17727673.001).
  • [ISSN] 0014-2972
  • [Journal-full-title] European journal of clinical investigation
  • [ISO-abbreviation] Eur. J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Benzamides; 0 / Liposomes; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 04079A1RDZ / Cytarabine; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
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7. Morimoto A, Ogami A, Chiyonobu T, Takanashi M, Sugimoto T, Imamura T, Ishida H, Yoshihara T, Imashuku S: Early blastic transformation following complete cytogenetic response in a pediatric chronic myeloid leukemia patient treated with imatinib mesylate. J Pediatr Hematol Oncol; 2004 May;26(5):320-2
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  • [Title] Early blastic transformation following complete cytogenetic response in a pediatric chronic myeloid leukemia patient treated with imatinib mesylate.
  • This article reports early blastic transformation of chronic myeloid leukemia (CML) in a child following a complete cytogenetic response induced by imatinib mesylate.
  • A 14-year-old Japanese boy was diagnosed with t(9;22) cryptic CML in the chronic phase and treated with imatinib.
  • His response to treatment was slow, but a major cytogenetic response was obtained at 142 days of therapy.
  • However, he developed lymphoid blastic transformation at 9 months.
  • He attained remission with acute lymphoblastic leukemia-type chemotherapy and then successfully received a non-T-cell-depleted allogeneic stem cell transplantation (allo-SCT) with his mother's two loci-mismatched donor cells.
  • A sudden blastic transformation may occur even with a complete cytogenetic response induced by imatinib.
  • [MeSH-major] Blast Crisis / therapy. Leukemia, Myeloid, Chronic-Phase / drug therapy. Lymphocyte Activation. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 15111787.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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8. Poulain S, Lepelley P, Preudhomme C, Cambier N, Cornillon J, Wattel E, Cosson A, Fenaux P: Expression of the multidrug resistance-associated protein in myelodysplastic syndromes. Br J Haematol; 2000 Sep;110(3):591-8
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  • In the myelodysplastic syndromes (MDS), P-glycoprotein (P-gp) expression is clinically associated with drug resistance, whereas the clinical significance of multidrug resistance-associated protein (MRP1) is uncertain.
  • Bone marrow from 56 patients with MDS, including six with refractory anaemia (RA)/RA with ringed sideroblasts (RARS), 23 cases of RA with excess blasts/in transformation (RAEB/T), four patients with chronic myelomonocytic leukaemia (CMML) and 23 cases of MDS having progressed to acute myeloid leukaemia (MDS-AML), were studied.
  • Ten of the 26 patients treated with intensive chemotherapy achieved complete remission including six out of 16 MRP1+ and four out of ten MRP1- cases (P = NS).
  • [MeSH-minor] ATP-Binding Cassette, Sub-Family B, Member 1 / analysis. Adult. Animals. Antigens, CD34 / analysis. Cell Line. Chi-Square Distribution. Chromosome Aberrations / metabolism. Chromosome Disorders. Flow Cytometry. Humans. Immunohistochemistry / methods. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / metabolism. Middle Aged. Multidrug Resistance-Associated Proteins. Neoplasm Proteins / analysis. Treatment Outcome. Vault Ribonucleoprotein Particles


9. Grzybowska-Izydorczyk O, Góra-Tybor J, Robak T: [Tyrosine kinase inhibitors in the therapy of chronic myeloid leukaemia]. Postepy Hig Med Dosw (Online); 2006;60:490-7
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  • [Title] [Tyrosine kinase inhibitors in the therapy of chronic myeloid leukaemia].
  • Chronic myeloid leukemia (CML) is a malignant clonal disorder of hematopoietic stem cells resulting in increased myeloid and erythroid cells and platelets, and marked hyperplasia in the bone marrow.
  • The natural history of CML is progression from a benign chronic phase, often through an accelerated phase, to a rapidly fatal blast crisis within 3-5 years.
  • The constitutively activated ABL tyrosine kinase domain of the chimeric BCR-ABL oncoprotein is responsible for the transformation of hematopoietic stem cells and the symptoms of CML.
  • Imatinib mesylate (Glivec), a specific small-molecule inhibitor of BCR-ABL, has become the standard drug therapy in all phases of the disease.
  • 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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10. Wadhwa J, Szydlo RM, Apperley JF, Chase A, Bua M, Marin D, Olavarria E, Kanfer E, Goldman JM: Factors affecting duration of survival after onset of blastic transformation of chronic myeloid leukemia. Blood; 2002 Apr 1;99(7):2304-9
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  • [Title] Factors affecting duration of survival after onset of blastic transformation of chronic myeloid leukemia.
  • We analyzed factors having an impact on response to treatment and survival in 78 consecutive patients with chronic myeloid leukemia (CML) in blastic transformation (BT) referred to the Hammersmith Hospital from January 1995 to December 2000.
  • Immunophenotyping of blasts showed 57 myeloid, 19 lymphoid, and 2 biphenotypic.
  • Patients in lymphoid BT survived longer than those in myeloid BT (median, 11.2 months versus 6.9 months, P =.052).
  • Initial treatment varied; 41 patients received cytotoxic drugs, 8 underwent allogeneic or autologous transplantation procedures, 21 received STI571 (imatinib mesylate, Gleevec), 1 received radiotherapy, and 7 received no therapy.
  • Of the 25 (32%) patients who achieved a "second chronic phase" with first therapy, 6 of 21 (29%) were treated with STI571 and 19 of 50 (38%) were treated with chemotherapy, transplantation, or radiotherapy.
  • Patients who achieved a second chronic phase survived longer than those who did not (median time from onset of BT 12.0 months versus 6.3 months, P =.0004).
  • We speculate that the combined use of STI571 with cytotoxic drugs may offer additional benefit.
  • [MeSH-major] Blast Crisis / mortality. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / therapeutic use. Child. Disease-Free Survival. Humans. Leukocyte Count. Middle Aged. Platelet Count. Predictive Value of Tests. Prognosis. Survival Rate. Time Factors


11. Roy S, Szer J, Campbell LJ, Juneja S: Sequential transformation of t(8;13)-related disease: a case report. Acta Haematol; 2002;107(2):95-7
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  • [Title] Sequential transformation of t(8;13)-related disease: a case report.
  • We report a case of an atypical myeloproliferative disorder with t(8;13) that presented as B-lineage acute lymphoblastic leukaemia (B-ALL).
  • Following induction chemotherapy, the disease manifested as chronic myeloproliferative state, which responded to hydroxyurea.
  • Terminally, the disease transformed into acute myeloid leukaemia (AML) with additional chromosomal abnormalities including monosomy 7.
  • To our knowledge, this is the first case of this rare atypical myeloproliferative disorder with t(8;13) that presented as B-ALL and terminally transformed to AML with additional chromosomal abnormalities.
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Transformation, Neoplastic / pathology. Chromosomes, Human, Pair 13. Chromosomes, Human, Pair 8. Myeloproliferative Disorders / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Aged. Cell Lineage. Diagnosis, Differential. Female. Humans. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology

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  • [Copyright] Copyright 2002 S. Karger AG, Basel
  • (PMID = 11919389.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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12. Banerji L, Sattler M: Targeting mutated tyrosine kinases in the therapy of myeloid leukaemias. Expert Opin Ther Targets; 2004 Jun;8(3):221-39
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  • [Title] Targeting mutated tyrosine kinases in the therapy of myeloid leukaemias.
  • Myeloid leukaemias are frequently associated with translocations and mutations of tyrosine kinase genes.
  • Activated ABL kinases are associated with chronic myeloid leukaemia.
  • Mutations in platelet-derived growth factor receptor beta are associated with chronic myelomonocytic leukaemia.
  • Flt3 or c-Kit cooperate with other types of oncogenes to create fully transformed acute leukaemias.
  • Elevated activity of these tyrosine kinases is crucial for transformation, thus making the kinase domain an ideal target for therapeutic intervention.
  • Tyrosine kinase inhibitors for various kinases are currently being evaluated in clinical trials and are potentially useful therapeutic agents in myeloid leukaemias.
  • Here, the authors review the signalling activities, mechanism of transformation and therapeutic targeting of several tyrosine kinase oncogenes important in myeloid leukaemias.
  • [MeSH-major] Drug Delivery Systems / methods. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / enzymology. Mutation. Protein-Tyrosine Kinases / genetics

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  • (PMID = 15161429.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 253
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13. Bright SA, Greene LM, Greene TF, Campiani G, Butini S, Brindisi M, Lawler M, Meegan MJ, Williams DC, Zisterer DM: The novel pyrrolo-1,5-benzoxazepine, PBOX-21, potentiates the apoptotic efficacy of STI571 (imatinib mesylate) in human chronic myeloid leukaemia cells. Biochem Pharmacol; 2009 Feb 1;77(3):310-21
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  • [Title] The novel pyrrolo-1,5-benzoxazepine, PBOX-21, potentiates the apoptotic efficacy of STI571 (imatinib mesylate) in human chronic myeloid leukaemia cells.
  • The Bcr-Abl kinase inhibitor, STI571, is the first line treatment for chronic myeloid leukaemia (CML), but the recent emergence of STI571 resistance has led to the examination of combination therapies.
  • Co-treatment of CML cells with PBOX-21 and STI571 induced more apoptosis than either drug alone in parental (K562S and LAMA84) and STI571-resistant cells lines (K562R).
  • This potentiation of apoptosis was specific to Bcr-Abl-positive leukaemia cells with no effect observed on Bcr-Abl-negative HL-60 acute myeloid leukaemia cells.
  • Repression of proteins involved in Bcr-Abl transformation, the anti-apoptotic proteins Mcl-1 and Bcl-(XL) was also observed.
  • Apoptosis was significantly reduced following pre-treatment with either the general caspase inhibitor Boc-FMK or the chymotrypsin-like serine protease inhibitor TPCK, but was completely abrogated following pre-treatment with a combination of these inhibitors.
  • In conclusion, our data highlights the potential of PBOX-21 in combination with STI571 as an effective therapy against CML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Carbamates / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Oxazepines / therapeutic use. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Blotting, Western. Cell Line, Tumor. Down-Regulation. Drug Synergism. Flow Cytometry. Fusion Proteins, bcr-abl / metabolism. Humans. Imatinib Mesylate. Membrane Potentials / drug effects. Up-Regulation

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  • (PMID = 19014913.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 7-((diethylcarbamoyl)oxy)-6-p-tolylpyrrolo(2,1-d)(1,5)benzoxazepine; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Carbamates; 0 / Oxazepines; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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14. Apfelbeck U, Hoefler G, Neumeister P, Fonatsch C, Linkesch W, Sill H: Extramedullary T cell lymphoblastic transformation of chronic myeloid leukaemia successfully treated with matched unrelated donor bone marrow transplantation. Bone Marrow Transplant; 2000 Nov;26(10):1111-2
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  • [Title] Extramedullary T cell lymphoblastic transformation of chronic myeloid leukaemia successfully treated with matched unrelated donor bone marrow transplantation.
  • Chronic myeloid leukaemia (CML) inevitably terminates in blast crisis (BC) which is of myeloid phenotype in approximately two-thirds and B-lymphoid in one-third of patients.
  • We describe the case of a 48-year-old woman with extramedullary T cell lymphoblastic transformation.
  • After treatment with combination chemotherapy she achieved a second chronic phase and underwent an allogeneic BMT from an HLA-matched unrelated donor.
  • We conclude that unrelated donor BMT should be considered as a therapeutic option for patients with extramedullary BC.
  • [MeSH-major] Blast Crisis / therapy. Bone Marrow Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. T-Lymphocytes / pathology


15. Pawson R, Potter MN, Theocharous P, Lawler M, Garg M, Yin JA, Rezvani K, Craddock C, Rassam S, Prentice HG: Treatment of relapse after allogeneic bone marrow transplantation with reduced intensity conditioning (FLAG +/- Ida) and second allogeneic stem cell transplant. Br J Haematol; 2001 Dec;115(3):622-9
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  • [Title] Treatment of relapse after allogeneic bone marrow transplantation with reduced intensity conditioning (FLAG +/- Ida) and second allogeneic stem cell transplant.
  • Acute leukaemias in relapse after allogeneic stem cell transplantation (SCT) respond poorly to donor leucocyte infusions (DLI) compared with chronic myeloid leukaemia (CML), at least in part because of faster disease kinetics.
  • Fludarabine-containing 'non-myeloablative' chemotherapy followed by further allo SCT may offer more rapid and effective disease control.
  • We report 14 patients with relapse after allo SCT for acute leukaemia [seven acute myeloid leukaemia (AML), five acute lymphoblastic leukaemia (ALL)] or refractory anaemia with excess blasts in transformation (RAEB-t, n = 2) treated with fludarabine, high-dose cytosine arabinoside (ara-C) and granulocyte colony-simulating factor (G-CSF) with (n = 10) or without (n = 2) idarubicin (FLAG +/- Ida) or DaunoXome (FLAG-X) (n = 2) and second allo SCT from the original donor.
  • Transplants were well tolerated with no treatment-related deaths.
  • The major complication was graft-versus-host disease (GvHD, acute >/= grade II-2 cases, chronic - eight cases, two limited, six extensive) although there have been no deaths attributable to this.
  • FLAG +/- Ida and second allo SCT is a safe and useful approach and may be more effective than DLI in the treatment of acute leukaemias relapsing after conventional allo SCT.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Bone Marrow Transplantation. Cytarabine / administration & dosage. Granulocyte Colony-Stimulating Factor / administration & dosage. Idarubicin / administration & dosage. Leukemia / therapy. Transplantation Conditioning / methods. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adult. Anemia, Refractory, with Excess of Blasts / therapy. Child. Child, Preschool. Disease-Free Survival. Female. Filgrastim. Graft vs Host Disease / immunology. Graft vs Host Disease / prevention & control. Humans. Leukemia, Myeloid / therapy. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Recombinant Proteins. Recurrence. Reoperation. Retrospective Studies. Survival Rate. Transplantation, Homologous

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  • (PMID = 11736947.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; PVI5M0M1GW / Filgrastim; ZRP63D75JW / Idarubicin; Ida-FLAG protocol
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16. Molnár L, Losonczy H: [Tyrosine kinase inhibitor STI571: new possibility in the treatment of chronic myeloid leukemia]. Orv Hetil; 2002 Oct 20;143(42):2379-84
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  • [Title] [Tyrosine kinase inhibitor STI571: new possibility in the treatment of chronic myeloid leukemia].
  • [Transliterated title] Uj lehetóség a krónikus myeloid leukaemia kezelésében: specifikus tirozinkináz-inhibitor (STI571).
  • Chronic myeloid leukemia shown to be associated with the Ph translocation,--characterised as a t(9;22)--, joins the bcr and abl genes and leads to expression of chimeric BCR-ABL protein with enhanced tyrosine kinase (TK) activity.
  • This increased TK activity leads to malignant transformation by interference with the control of proliferation, cellular adherence and apoptosis.
  • Following this observations efforts were made to develop molecularly targeted therapies for CML.
  • The specific inhibitor of BCR-ABL TK, STI571 was developed by Brian Druker and his co-workers in 1996.
  • Patients with chronic phase after failure with interferon therapy achieved more than 90% hematologic response, usually within 4-6 weeks, and 55% major cytogenetic response.
  • In phase 2 studies the drug has continued to produce impressive results.
  • STI571 has a very favourable pharmacologic feature, with high degree of specificity for its target, and therefore low toxicity for normal tissues, it is well tolerable, side effects were minimal.
  • STI571 opens a new era in the treatment of malignancies, it is the first targeted molecular therapy which is able to target abnormal cells without damaging normal cells, compared with traditional antineoplastic drugs.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Enzyme Inhibitors / pharmacology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Benzamides. Cell Division / drug effects. Cell Transformation, Neoplastic / drug effects. Drug Resistance, Neoplasm. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Phosphorylation / drug effects. Signal Transduction / drug effects

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  • (PMID = 12440260.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 34
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17. Chien RN, Yeh CT, Wang PN, Kuo MC, Hsieh SY, Shih LY, Liaw YF: Acute leukaemia in chronic hepatitis B patients with lamivudine therapy. Int J Clin Pract; 2004 Nov;58(11):1088-91
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  • [Title] Acute leukaemia in chronic hepatitis B patients with lamivudine therapy.
  • Extensive clinical data have shown that lamivudine is an effective and safe drug for patients with chronic hepatitis B virus infection.
  • Four hundred and forty-eight patients with chronic hepatitis B, treated with lamivudine for more than 6 months, were closely monitored.
  • Two patients developed acute myeloid leukaemia during or after lamivudine therapy.
  • The first case developed acute myeloid leukaemia, 1 year after stopping lamivudine therapy, when A529T mutant HBV-DNA was still detectable.
  • The second case achieved complete virological response but suffered from acute myeloid leukaemia during the ninth month of lamivudine treatment.
  • Based on our lamivudine therapy data, the calculated incidence of acute myeloid leukaemia in patients during or after lamivudine therapy was higher in males and females than that of the general population.
  • Whether lamivudine-selected viral mutations have enhanced activity/production of transcriptional transactivator and thereby increased the chance of leukaemic transformation of haematopoietic progenitor cells deserves further investigation.
  • [MeSH-major] Hepatitis B, Chronic / drug therapy. Lamivudine / adverse effects. Leukemia, Myeloid / chemically induced. Reverse Transcriptase Inhibitors / adverse effects

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  • (PMID = 15605678.001).
  • [ISSN] 1368-5031
  • [Journal-full-title] International journal of clinical practice
  • [ISO-abbreviation] Int. J. Clin. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Reverse Transcriptase Inhibitors; 2T8Q726O95 / Lamivudine
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18. Markert E, Siebolts U, Odenthal M, Kreuzer KA, Wickenhauser C: High diagnostic value of morphologic examination and molecular analysis of bone marrow biopsies in a case of BCR-ABL+ CML with clusters of blasts. Int J Hematol; 2009 Apr;89(3):294-7
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  • We report a clinical case of chronic myelogenous leukaemia (CML) with regional B-lymphoblastic transformation.
  • In peripheral blood and bone marrow smears, white blood cells in all maturation stages and only few blasts were seen and therefore the diagnosis of chronic phase CML was proposed.
  • BCR-ABL FISH analysis demonstrated 31% atypical split signals in the B-lymphoid blasts and in the maturing myeloid cells, furthermore, BCR-ABL fusion transcripts were seen in the RT-PCR assay.
  • Imatinib-based therapy led to temporary regression of peripheral leukocytosis.
  • Bone marrow examination 3 weeks after therapy induction demonstrated considerably reduced cellularity and the proportion of B-lymphoid blasts had decreased to 20% of the nuclear cells.
  • However, 3 months after diagnosis the patient relapsed and developed an immunodeficiency with soor esophagitis and aspergillus pneumonia.
  • A therapy with dasatinib was not successful and the patient died in consequence of immunodeficiency.
  • Besides morphology investigation of diverse methods including RT-PCR and FISH performed on diagnostic bone marrow biopsies are obligatory for ideal monitoring of drug response.
  • [MeSH-major] Bone Marrow / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism

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  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
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19. Perrotti D, Neviani P: ReSETting PP2A tumour suppressor activity in blast crisis and imatinib-resistant chronic myelogenous leukaemia. Br J Cancer; 2006 Oct 9;95(7):775-81
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  • [Title] ReSETting PP2A tumour suppressor activity in blast crisis and imatinib-resistant chronic myelogenous leukaemia.
  • The deregulated kinase activity of p210-BCR/ABL oncoproteins, hallmark of chronic myelogenous leukaemia (CML), induces and sustains the leukaemic phenotype, and contributes to disease progression.
  • Imatinib mesylate, a BCR/ABL kinase inhibitor, is effective in most of chronic phase CML patients.
  • However, a significant percentage of CML patients develop resistance to imatinib and/or still progresses to blast crisis, a disease stage that is often refractory to imatinib therapy.
  • Furthermore, there is compelling evidence indicating that the CML leukaemia stem cell is also resistant to imatinib.
  • Thus, there is still a need for new drugs that, if combined with imatinib, will decrease the rate of relapse, fully overcome imatinib resistance and prevent blastic transformation of CML.
  • We recently reported that the activity of the tumour suppressor protein phosphatase 2A (PP2A) is markedly inhibited in blast crisis CML patient cells and that molecular or pharmacologic re-activation of PP2A phosphatase led to growth suppression, enhanced apoptosis, impaired clonogenic potential and decreased in vivo leukaemogenesis of imatinib-sensitive and -resistant (T315I included) CML-BC patient cells and/or BCR/ABL+ myeloid progenitor cell lines.
  • Thus, the combination of PP2A phosphatase-activating and BCR/ABL kinase-inhibiting drugs may represent a powerful therapeutic strategy for blast crisis CML patients.

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  • (PMID = 16953242.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / CA095512
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / Protein Phosphatase 2
  • [Number-of-references] 74
  • [Other-IDs] NLM/ PMC2360538
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20. McGrattan P, Humphreys M, Hull D, McMullin MF: Transformation of cytogenetically normal chronic myelomonocytic leukaemia to an acute myeloid leukaemia and the emergence of a novel +13, +15 double trisomy resulting in an adverse outcome. Ulster Med J; 2007 Sep;76(3):131-5
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  • [Title] Transformation of cytogenetically normal chronic myelomonocytic leukaemia to an acute myeloid leukaemia and the emergence of a novel +13, +15 double trisomy resulting in an adverse outcome.
  • Peripheral blood (PB) analysis revealed a white blood cell count (WBC) of 15.9 x 10(9)/l with monocytes 5.4 x 10(9)/l.
  • A diagnosis of chronic myelomonocytic leukaemia (CMML) was made.
  • BM aspirate analysis also revealed 89% myeloid blasts and G-banding detected the emergence of an abnormal clone harbouring an extra copy of chromosomes 13 and 15.
  • A diagnosis of disease transformation to acute myeloid leukaemia (AML) was made.
  • Post chemotherapy BM aspirate was very hypocellular and the abnormal +13, +15 clone was still present suggesting primary refractory disease.
  • A second course of chemotherapy was only administered for 24 hours due to complications.
  • The abnormal +13, +15 clone was still present and it was decided that no further treatment apart from palliative care could be offered.
  • The patient died 11 weeks later, five months after AML transformation.
  • [MeSH-major] Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 15 / genetics. Leukemia, Myeloid / genetics. Leukemia, Myelomonocytic, Chronic / genetics. Trisomy / genetics
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / therapeutic use. Cytogenetics. Fatal Outcome. Humans. Male. Middle Aged. Treatment Outcome

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  • (PMID = 17853637.001).
  • [ISSN] 0041-6193
  • [Journal-full-title] The Ulster medical journal
  • [ISO-abbreviation] Ulster Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Northern Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Other-IDs] NLM/ PMC2075573
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21. Chávez-González MA, Ayala-Sánchez M, Mayani H: [Chronic myeloid leukemia in the 21st century: biology and treatment]. Rev Invest Clin; 2009 May-Jun;61(3):221-32
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  • [Title] [Chronic myeloid leukemia in the 21st century: biology and treatment].
  • [Transliterated title] La leucemia mieloide crónica en el siglo XXI: biología y tratamiento.
  • Chronic Myeloid Leukaemia (CML) is a clonal disease, originated at the level of Hematopoietic Stem Cells (HSC) and characterized by the presence of the Philadelphia (Ph) chromosome and its oncogenic product p210(BcrAbl).
  • Such a protein has been shown to be essential for malignant transformation, since it is capable of altering cell adhesion, proliferation and apoptosis.
  • Historically, CML has been treated by using different approaches: arsenic (in the early days), a variety of chemical agents (busulfan, hydroxyurea, cytarabine), cytokines (IFN-alpha, IFNalpha-PEG), hematopoietic cell transplant (HCT), and more recently drugs generated by design (imatinib, nilotinib, dasatinib).
  • In this article, we present an overview about hematopoiesis in CML and its implications in the treatment of this disease.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Drug Design. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / genetics. Hematopoiesis / drug effects. Hematopoiesis / physiology. Hematopoietic Stem Cell Transplantation. Hematopoietic Stem Cells / drug effects. Hematopoietic Stem Cells / pathology. Humans. Immunologic Factors / therapeutic use. Incidence. Interferon-alpha / therapeutic use. Mexico / epidemiology. Middle Aged. Neoplastic Stem Cells / drug effects. Neoplastic Stem Cells / pathology. Protein Kinase Inhibitors / therapeutic use. United States / epidemiology

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  • (PMID = 19736811.001).
  • [ISSN] 0034-8376
  • [Journal-full-title] Revista de investigación clínica; organo del Hospital de Enfermedades de la Nutrición
  • [ISO-abbreviation] Rev. Invest. Clin.
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunologic Factors; 0 / Interferon-alpha; 0 / Protein Kinase Inhibitors; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 81
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22. Löfström B, Backlin C, Sundström C, Hellström-Lindberg E, Ekbom A, Lundberg IE: Myeloid leukaemia in systemic lupus erythematosus--a nested case-control study based on Swedish registers. Rheumatology (Oxford); 2009 Oct;48(10):1222-6
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  • [Title] Myeloid leukaemia in systemic lupus erythematosus--a nested case-control study based on Swedish registers.
  • OBJECTIVE: To assess the risk factors for leukaemic transformation and myeloid leukaemia in patients with SLE.
  • A nested case-control study in SLE patients who developed acute or chronic myeloid leukaemia was performed with SLE patients without malignancy as controls.
  • A Medline search of previously published cases of SLE and myeloid leukaemia was performed.
  • RESULTS: After confirmation of SLE diagnosis according to the ACR criteria, eight patients with SLE and myeloid leukaemia and 18 SLE controls were included in the study.
  • Preceding leucopenia was significantly associated with leukaemia development, whereas other SLE manifestations were not.
  • A Medline search resulted in only 15 previously published cases of coincident SLE and myeloid leukaemia.
  • Preceding MDS was reported in five of these, whereas only eight had been treated with cytotoxic drugs.
  • CONCLUSION: Low-dose chemotherapy was not a major cause of myeloid malignancy in our population-based cohort of SLE patients nor in the reported cases from literature.
  • Leucopenia was a risk factor for myeloid leukaemia development and an MDS was frequently seen.
  • [MeSH-major] Leukemia, Myeloid / etiology. Leukemia, Myeloid, Acute / etiology. Lupus Erythematosus, Systemic / complications
  • [MeSH-minor] Adolescent. Adult. Aged. Bone Marrow Examination / methods. Epidemiologic Methods. Female. Humans. Immunosuppressive Agents / adverse effects. Immunosuppressive Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / epidemiology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / etiology. Leukopenia / complications. Leukopenia / epidemiology. Male. Middle Aged. Phenotype. Sweden / epidemiology. Young Adult


23. Joske DJ: Chronic myeloid leukaemia: the evolution of gene-targeted therapy. Med J Aust; 2008 Sep 01;189(5):277-82
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  • [Title] Chronic myeloid leukaemia: the evolution of gene-targeted therapy.
  • Chronic myeloid leukaemia (CML) was the first human cancer linked to an acquired chromosomal abnormality, subsequently shown to be a reciprocal translocation between chromosomes 9 and 22.
  • Treatment of CML with imatinib has been a powerful vindication of the concept of rational, gene-targeted drug design.
  • Bone marrow transplantation remains the only known cure, but is reserved for patients whose kinase inhibitor therapy has failed, or who have advanced disease (accelerated phase or blastic transformation).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Australia. Benzamides. Drug Approval. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / genetics. Humans. Imatinib Mesylate. United States

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  • (PMID = 18759727.001).
  • [ISSN] 0025-729X
  • [Journal-full-title] The Medical journal of Australia
  • [ISO-abbreviation] Med. J. Aust.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 41
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24. Manley PW, Cowan-Jacob SW, Mestan J: Advances in the structural biology, design and clinical development of Bcr-Abl kinase inhibitors for the treatment of chronic myeloid leukaemia. Biochim Biophys Acta; 2005 Dec 30;1754(1-2):3-13
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  • [Title] Advances in the structural biology, design and clinical development of Bcr-Abl kinase inhibitors for the treatment of chronic myeloid leukaemia.
  • The constitutively activated Abl tyrosine kinase domain of the chimeric Bcr-Abl oncoprotein is responsible for the transformation of haematopoietic stem cells and the symptoms of chronic myeloid leukaemia (CML).
  • Imatinib targets the tyrosine kinase activity of Bcr-Abl and is a first-line therapy for this malignancy.
  • Although highly effective in chronic phase CML, patients who have progressed to the advanced phase of the disease frequently fail to respond to imatinib or develop resistance to therapy and relapse.
  • 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 BMS-354825 (BristolMyersSquibb) and AMN107 (Novartis Pharma) and, from Phase I results, both of these promise a breakthrough in the treatment of imatinib-resistant CML.
  • Recent advances with these and other promising classes of new CML drugs are reviewed.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Design. Enzyme Inhibitors / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Benzamides. Clinical Trials as Topic. Drug Evaluation, Preclinical. Drug Resistance, Neoplasm. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Mutation. Piperazines / pharmacology. Piperazines / therapeutic use. Pyrimidines / pharmacology. Pyrimidines / therapeutic use

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  • (PMID = 16172030.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 75
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