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1. Ding JH, Ma Y, Chen BA, Zhao G, Wang J, Sun YY, Cheng J, Su AL, Dong WM, Zhang Y: [Nonmyeloablative peripheral blood stem cell transplantation for chronic myeloid leukemia in chronic and accelerated phases]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Apr;16(2):373-6
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  • [Title] [Nonmyeloablative peripheral blood stem cell transplantation for chronic myeloid leukemia in chronic and accelerated phases].
  • The aim of this study was to investigate the effect of nonmyeloablative peripheral blood stem cell transplantation in treatment of chronic myeloid leukemia in chronic phase (CML-CP) and accelerated phase (CML-AP).
  • 24 patients with CML including 16 in CML-CP and 8 in CML-AP were treated with nonmyeloablative conditioning regimen for peripheral blood stem cell transplantation (PBHSCT).
  • 2 cases died of severe acute GVHD and 1 case died of chronic GVHD, 2 cases died of interstitial pneumonia and 1 case died of relapsed.
  • In conclusions, nonmyeloablative peripheral blood stem cell transplantation is an effective therapeutic method for CML patients in chronic phase and accelerated phase.



2. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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3. Krejci M, Mayer J, Doubek M, Brychtova Y, Pospisil Z, Racil Z, Dvorakova D, Lengerova M, Horky O, Koristek Z, Dolezal T, Vorlicek J: Clinical outcomes and direct hospital costs of reduced-intensity allogeneic transplantation in chronic myeloid leukemia. Bone Marrow Transplant; 2006 Oct;38(7):483-91
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  • [Title] Clinical outcomes and direct hospital costs of reduced-intensity allogeneic transplantation in chronic myeloid leukemia.
  • A reduced-intensity conditioning allogeneic stem cell transplantation was given to 19 patients (aged 15-59 years) in the first chronic phase and one patient in the accelerated phase with chronic myeloid leukemia (CML) after a regimen consisting of fludarabine (Flu), busulfan (Bu) and ATG Fresenius.
  • The incidence of acute and chronic graft-versus-host disease (GvHD) was 55 and 75%, respectively.
  • Flu+Bu+ATG is a low-toxicity regimen for patients with CML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation / economics. Hospital Costs / statistics & numerical data. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Transplantation Conditioning
  • [MeSH-minor] Adolescent. Adult. Antilymphocyte Serum / administration & dosage. Busulfan / administration & dosage. Czech Republic. Female. Graft vs Host Disease / prevention & control. Humans. Male. Middle Aged. Myeloablative Agonists / administration & dosage. Philadelphia Chromosome. Retrospective Studies. Survival Analysis. Transplantation, Homologous / economics. Transplantation, Homologous / methods. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives



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4. 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



5. Soverini S, Martinelli G, Rosti G, Bassi S, Amabile M, Poerio A, Giannini B, Trabacchi E, Castagnetti F, Testoni N, Luatti S, de Vivo A, Cilloni D, Izzo B, Fava M, Abruzzese E, Alberti D, Pane F, Saglio G, Baccarani M: ABL mutations in late chronic phase chronic myeloid leukemia patients with up-front cytogenetic resistance to imatinib are associated with a greater likelihood of progression to blast crisis and shorter survival: a study by the GIMEMA Working Party on Chronic Myeloid Leukemia. J Clin Oncol; 2005 Jun 20;23(18):4100-9
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  • [Title] ABL mutations in late chronic phase chronic myeloid leukemia patients with up-front cytogenetic resistance to imatinib are associated with a greater likelihood of progression to blast crisis and shorter survival: a study by the GIMEMA Working Party on Chronic Myeloid Leukemia.
  • PURPOSE: Point mutations within the ABL kinase domain of the BCR-ABL gene have been associated with clinical resistance to imatinib mesylate in chronic myeloid leukemia (CML) patients.
  • To shed further light on the frequency, distribution, and prognostic significance of ABL mutations, we retrospectively analyzed a homogeneous cohort of late chronic phase CML patients who showed primary cytogenetic resistance to imatinib.
  • PATIENTS AND METHODS: Using denaturing high-performance liquid chromatography (D-HPLC) and sequencing, we screened for ABL mutations in a total of 178 bone marrow and/or peripheral blood samples from 40 late chronic phase CML patients homogeneously treated with imatinib 400 mg/d, who did not reach a major cytogenetic response at 12 months.
  • The presence of a missense mutation was significantly associated with a greater likelihood of subsequent progression to accelerated phase/blast crisis (P = .0002) and shorter survival (P = .001).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cytogenetic Analysis / methods. Drug Resistance, Neoplasm / genetics. Genes, abl / genetics. Leukemia, Myeloid, Chronic-Phase / genetics. Piperazines / therapeutic use. Point Mutation. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Aged. Benzamides. Blast Crisis. Chi-Square Distribution. Chromatography, High Pressure Liquid. DNA Mutational Analysis. Disease Progression. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric. Survival Analysis

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  • (PMID = 15867198.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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6. 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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7. Mauro MJ: Tailoring tyrosine kinase inhibitor therapy in chronic myeloid leukemia. Cancer Control; 2009 Apr;16(2):108-21
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  • [Title] Tailoring tyrosine kinase inhibitor therapy in chronic myeloid leukemia.
  • BACKGROUND: Research into chronic myeloid leukemia (CML) is increasingly focused on the problem of imatinib failure.
  • Dasatinib and nilotinib are both active in chronic- and accelerated-phase CML, including patients with imatinib-resistant or intolerant disease.
  • METHODS: This paper reviews advances in tailoring tyrosine kinase inhibition therapy according to patient risk profiles as well as hematologic, cytogenetic, and molecular responses, BCR-ABL mutation status, and emerging predictive factors.
  • CONCLUSIONS: Treatment for CML should be individualized and, when resistance to imatinib can be predicted, therapy should be modified so that patients do not progress beyond chronic phase and respond as promptly and deeply as required to maximally reduce risk.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / genetics

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  • (PMID = 19337197.001).
  • [ISSN] 1526-2359
  • [Journal-full-title] Cancer control : journal of the Moffitt Cancer Center
  • [ISO-abbreviation] Cancer Control
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; RBZ1571X5H / Dasatinib
  • [Number-of-references] 118
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8. Agis H, Krauth MT, Mosberger I, Müllauer L, Simonitsch-Klupp I, Schwartz LB, Printz D, Böhm A, Fritsch G, Horny HP, Valent P: Enumeration and immunohistochemical characterisation of bone marrow basophils in myeloproliferative disorders using the basophil specific monoclonal antibody 2D7. J Clin Pathol; 2006 Apr;59(4):396-402
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  • In chronic myeloid leukaemia (CML), basophilia is a diagnostic and prognostic determinant.
  • OBJECTIVE: To detect and enumerate basophils in bone marrow sections in patients with CML and other MPD.
  • METHODS: The anti-basophil antibody 2D7 was applied to paraffin embedded bone marrow sections from normal/reactive subjects (n = 31), patients with CML (chronic phase, n = 37; accelerated phase, n = 9), and other MPD (chronic idiopathic myelofibrosis (CIMF), n = 20; polycythaemia vera (PV), n = 20; essential thrombocythaemia (ET), n = 20; indolent systemic mastocytosis (ISM), n = 7).
  • 2D7(+) bone marrow cells were found to increase in CML compared with normal/reactive bone marrow and other MPD (median numbers of 2D7(+) cells/mm(2): CML, 33; normal/reactive bone marrow, 6; CIMF, 10; PV, 6; ET, 5; ISM, 3; p<0.05).
  • The highest basophil counts were recorded in accelerated phase CML (115/mm(2)).
  • This approach should help in the quantification of bone marrow basophils at diagnosis and during anti-leukaemic treatment.

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  • [Cites] J Allergy Clin Immunol. 2002 Feb;109(2):287-93 [11842299.001]
  • [Cites] Blood. 2001 Dec 15;98(13):3784-92 [11739187.001]
  • [Cites] Scand J Haematol. 1977 Jan;18(1):25-38 [265093.001]
  • [Cites] J Clin Invest. 1980 Feb;65(2):390-9 [6965379.001]
  • [Cites] J Histochem Cytochem. 1981 Apr;29(4):577-80 [6166661.001]
  • [Cites] Cancer. 1981 May 15;47(10):2470-7 [6944141.001]
  • [Cites] Blood. 1982 Jul;60(1):113-20 [6952947.001]
  • [Cites] Fed Proc. 1983 May 15;42(8):2504-9 [6301890.001]
  • [Cites] Blood. 1984 Jul;64(1):78-83 [6234038.001]
  • [Cites] Am J Clin Pathol. 1984 Jul;82(1):1-14 [6588747.001]
  • [Cites] Prog Clin Biol Res. 1984;154:3-17 [6382299.001]
  • [Cites] J Immunol. 1986 May 1;136(9):3447-54 [3007619.001]
  • [Cites] Blood. 1987 Dec;70(6):1872-9 [3118989.001]
  • [Cites] Br J Haematol. 1987 Nov;67(3):281-4 [3479996.001]
  • [Cites] Cancer. 1988 Apr 1;61(7):1441-6 [3162181.001]
  • [Cites] Leukemia. 1988 Mar;2(3):141-3 [3258049.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2288-92 [3258425.001]
  • [Cites] J Med. 1987;18(5-6):293-303 [3505257.001]
  • [Cites] Blood. 1989 Feb 15;73(3):777-81 [2644988.001]
  • [Cites] Blood. 1989 May 15;73(7):1763-9 [2469498.001]
  • [Cites] Int Arch Allergy Appl Immunol. 1990;91(2):198-203 [1971264.001]
  • [Cites] Crit Rev Oncol Hematol. 1990;10(4):327-52 [2278641.001]
  • [Cites] Adv Immunol. 1992;52:333-423 [1332448.001]
  • [Cites] J Pathol. 1993 Oct;171(2):83-98 [7506771.001]
  • [Cites] Allergy. 1994 Dec;49(10):861-5 [7709996.001]
  • [Cites] J Immunol. 1995 Jun 15;154(12):6548-55 [7759888.001]
  • [Cites] Immunology. 1996 Apr;87(4):535-43 [8675206.001]
  • [Cites] Leuk Lymphoma. 1996 Jul;22(3-4):187-204 [8819068.001]
  • [Cites] Sao Paulo Med J. 1996 Jan-Feb;114(1):1083-90 [8984584.001]
  • [Cites] Int Rev Cytol. 1998;180:87-236 [9496635.001]
  • [Cites] J Allergy Clin Immunol. 1998 Mar;101(3):354-62 [9525452.001]
  • [Cites] J Natl Cancer Inst. 1998 Jun 3;90(11):850-8 [9625174.001]
  • [Cites] Am J Surg Pathol. 1998 Sep;22(9):1132-40 [9737247.001]
  • [Cites] Lab Invest. 1999 Jan;79(1):27-38 [9952108.001]
  • [Cites] Prog Histochem Cytochem. 1998;33(3-4):III-IX, 169-320 [10319376.001]
  • [Cites] Blood. 1999 Oct 1;94(7):2343-56 [10498606.001]
  • [Cites] Acta Med Scand. 1963 Aug;174:249-54 [14051143.001]
  • [Cites] Haematologica. 1999 Nov;84(11):978-87 [10553157.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4028-38 [11110670.001]
  • [Cites] Adv Immunol. 2001;77:93-122 [11293121.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3484-90 [11369641.001]
  • [Cites] Hum Pathol. 2001 May;32(5):545-52 [11381374.001]
  • [Cites] J Allergy Clin Immunol. 2001 Aug;108(2):205-11 [11496235.001]
  • [Cites] Clin Exp Allergy. 2001 Nov;31(11):1705-13 [11696046.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2292-302 [12239137.001]
  • (PMID = 16461568.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI020487; United States / NIAID NIH HHS / AI / R21 AI020487; United States / NIAID NIH HHS / AI / R37 AI020487; United States / NIAID NIH HHS / AI / AI20487
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers; 820484N8I3 / Histamine
  • [Other-IDs] NLM/ PMC1860377
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9. Bhattacharyya J, Mihara K, Yasunaga S, Tanaka H, Hoshi M, Takihara Y, Kimura A: BMI-1 expression is enhanced through transcriptional and posttranscriptional regulation during the progression of chronic myeloid leukemia. Ann Hematol; 2009 Apr;88(4):333-40
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  • [Title] BMI-1 expression is enhanced through transcriptional and posttranscriptional regulation during the progression of chronic myeloid leukemia.
  • Patients with chronic myeloid leukemia (CML) are at a risk of developing blastic crisis (BC) even after the emergence of imatinib mesylate.
  • In this study, to determine the relevance of BMI-1 to BC, we investigated the expression of BMI-1 in CD34(+) cells at each of the chronic phase (CP), the accelerated phase (AP), and BC by flow cytometry.
  • Interestingly, the level of BMI-1 expression was significantly higher in CP than in controls and was further increased during the course of the disease progression (control--5.66%; CP--36.93%; AP and BC--76.41%).
  • Curiously, mRNA levels for BMI-1 were almost consistent during the disease progression from CP to BC (control--2.21; CP--9.77; AP and BC--9.70 (BMI-1/glyceraldehyde-3-phosphate dehydrogenase ratio)).
  • Since we further found that overexpression of BCR-ABL in human embryonic kidney-293 cells enhanced BMI-1 expression and that BMI-1 expression was increased in K562 cells, derived from patients with BC, in the presence of proteasomal inhibitors, BMI-1 was presumed to be positively regulated by BCR-ABL and further by posttranscriptional modification in the course of the disease progression.
  • We suggest the usefulness of BMI-1 expression in CD34(+) cells as a molecular marker for monitoring patients with CML.
  • [MeSH-major] Blast Crisis / pathology. Gene Expression Regulation, Leukemic. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Nuclear Proteins / analysis. Proto-Oncogene Proteins / analysis. Repressor Proteins / analysis. Transcription, Genetic
  • [MeSH-minor] Antigens, CD34. Cell Line, Tumor. Disease Progression. Fusion Proteins, bcr-abl / physiology. Humans. Neoplastic Stem Cells / pathology. Polycomb Repressive Complex 1. RNA Processing, Post-Transcriptional

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  • (PMID = 18781299.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / BMI1 protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 6.3.2.19 / Polycomb Repressive Complex 1
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10. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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



11. 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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12. Fausel C: Targeted chronic myeloid leukemia therapy: seeking a cure. J Manag Care Pharm; 2007 Oct;13(8 Suppl A):8-12
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  • [Title] Targeted chronic myeloid leukemia therapy: seeking a cure.
  • BACKGROUND: Chronic myeloid leukemia (CML) is a hematopoietic stem cell cancer driven by the BCR-ABL fusion protein that arises from the translocation of chromosomes 9 and 22.
  • The disease begins with an indolent chronic phase (CP) that can last for 3 to 5 years.
  • If untreated, it progresses into accelerated phase (AP) and within a year, blast phase (BP).
  • Survival at this point is less than 1 year. during disease progression, mutations and the Philadelphia chromosome (Ph) appear (a process called clonal evolution).
  • The only known curative therapy for CML is allogeneic bone marrow transplant (BMT).
  • Thus, effective therapy that maintains the patient with CML in CP with minimal toxicity is the goal for treatment of modern therapies.
  • Because the preeminent mutation driving CML is BCr-ABL, therapies targeting BCR-ABL are the logical choice for disease-specific therapy.
  • BCR-ABL inhibitors, such as imatinib, are proof that targeting specific genetic mutations associated with cancer yields a high degree of efficacy with minimal toxicity.
  • OBJECTIVE: This review will outline the evolution of therapy in CML.
  • SUMMARY: The discovery of the Ph and, subsequently, the identification of BCr-ABL revolutionized the treatment of CML.
  • Cytoreductive chemotherapy, such as busulfan and hydroxyurea, was a mainstay of therapy to control white blood cell (WBC) counts; however, it did not modify the progression of the disease to AP and BP.
  • The overall survival with CML ranges from 45 to 58 months in patients treated with cytoreductive therapy only.
  • Allogeneic BMT is the only known curative therapy for CML; however, treatment-related mortality from infection, bleeding, and graft versus host disease, age, and the availability of suitable donors limits its widespread use.
  • Imatinib functions by competing with adenosine triphosphate (ATP) for binding to the BCr-ABL tyrosine kinase.
  • In the absence of ATP, BCR-ABL is not able to activate downstream effector tyrosine kinase molecules that drive wBC proliferation.
  • Toxicities associated with this therapy are low. response in patients with advanced CML is less pronounced than in CP and is shorter lived, with less than 30% of patients achieving a CHR.
  • For patients with CML in BP, the only viable therapy is to attempt a temporary reduction in disease burden with a salvage chemotherapy regimen, such as VAC (etoposide, cytarabine, and carboplatin).
  • Imatinib resistance may develop at any time and inevitably leads to disease progression. resistance is usually caused by mutations within BCr-ABL, decreasing the affinity of imatinib binding. next-generation kinase inhibitors are focused on the ability to inhibit these mutated forms of BCR-ABL.
  • CONCLUSION: For the majority of patients with CML in CP, the standard of care is to maintain the patient in CP with imatinib therapy.
  • Allogeneic BMT continues to be an option for those who cannot tolerate imatinib or when CML progresses on imatinib therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use



13. Liu L, Liu Q, Hao MW, Chen RA, Zhang JL, Wang LH, He H, Jiang SS, Liang YM: [Nonmyleoablative allogeneic stem cell transplantation combined with imatinib in treatment of chronic myeloid leukemia: a clinical study]. Zhonghua Yi Xue Za Zhi; 2005 Apr 27;85(16):1102-5
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  • [Title] [Nonmyleoablative allogeneic stem cell transplantation combined with imatinib in treatment of chronic myeloid leukemia: a clinical study].
  • OBJECTIVE: To study the effect of nonmyeloablative allogeneic peripheral blood stem cell (NST) transplantation combined with imatinib in the treatment of chronic myeloid leukemia (CML).
  • METHODS: Ten CML patients, 5 males and 5 females, aged 21-41, 3 in chronic phase (CP), 4 in accelerated phase (AP) and 3 in blast crisis phase (BP), were treated with imatinib (400-1500 mg/d) before (n = 10) and/or after (n = 6) NST transplantation.
  • Graft-versus-host disease (GVHD) prophylaxis consisted of cyclosporine (CSA) and mycophenolate mofetil (MMF), or with low-dose methotrexate (MTX) or zenapax.
  • 6 cases had I-II degrees acute and chronic GVHD of skin.
  • 2 case had III-IV degrees chronic GVHD.
  • The time needed for bcr/abl becoming negative was 33-130 days.
  • CONCLUSION: An effective and safer method for CML, especially advanced CML treatment of NST transplantation combined with imatinib before and after transplantation reduces the leukemic cell load before transplantation, inhibits the proliferation of residual leukemic cells, promotes full chimerism change and enhanced the effect of graft versus leukemia.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Peripheral Blood Stem Cell Transplantation. Piperazines / therapeutic use. Pyrimidines / therapeutic use



14. Lindauer M, Hochhaus A: Dasatinib. Recent Results Cancer Res; 2010;184:83-102
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  • 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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15. Zou WY, Xu DR, Su C, Chen M, Li J, Luo SK: [Dynamic observations of beta-catenin in chronic myeloid leukemia and its relationship with cytogenetic response]. Nan Fang Yi Ke Da Xue Xue Bao; 2010 Aug;30(8):1868-70, 1873
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  • [Title] [Dynamic observations of beta-catenin in chronic myeloid leukemia and its relationship with cytogenetic response].
  • OBJECTIVE: To investigate the changes in the expression of beta-catenin in patients with chronic myeloid leukemia (CML) in different phases, and explore the relationship between beta-catenin and the cytogenetic response to imatinib mesylate.
  • METHODS: Beta-catenin mRNA and protein expressions were detected by RT-PCR and Western blotting in the bone marrow mononuclear cells (BMMNCs) from 99 CML patients.
  • The expressions of BCR-ABL fusion gene at both the mRNA and protein levels were detected by fluorescence in situ hybridization (FISH) in 94 patients before and during the one-year treatment with imatinib mesylate at the interval of 3 months, and the relationship between beta-catenin and cytogenetic response to imatinib mesylate was analyzed.
  • RESULTS: The expression of beta-catenin increased significantly in patients with blast crisis and accelerated phase (P<0.001), but showed no significant difference between normal subjects and CML patients in the chronic phase (P>0.05).
  • The main cytogenetic remission rate was significantly higher in patients who were consistently negative for beta-catenin than in those consistently positive for beta-catenin or those with a positive transformation (P<0.001).
  • CONCLUSION: Beta-catenin overexpression in the progression of CML, consistent high level of beta-catenin or a positive transformation may indicate a poor response to imatinib, and early measures should be taken to increase the remission rate.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. beta Catenin / metabolism

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  • (PMID = 20813688.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Benzamides; 0 / CTNNB1 protein, human; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / beta Catenin; 8A1O1M485B / Imatinib Mesylate
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16. Kantarjian H, Talpaz M, O'Brien S, Giles F, Faderl S, Verstovsek S, Garcia-Manero G, Shan J, Rios MB, Champlin R, de Lima M, Cortes J: Survival benefit with imatinib mesylate therapy in patients with accelerated-phase chronic myelogenous leukemia--comparison with historic experience. Cancer; 2005 May 15;103(10):2099-108
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  • [Title] Survival benefit with imatinib mesylate therapy in patients with accelerated-phase chronic myelogenous leukemia--comparison with historic experience.
  • BACKGROUND: The effect of imatinib mesylate on survival in the accelerated phase of chronic myelogenous leukemia (CML) is unknown.
  • The objectives of this study were to update the long-term experience with imatinib in patients who had accelerated-phase CML and to compare outcomes with historic experience.
  • METHODS: The outcomes of 176 patients who received treatment with imatinib were reviewed and compared with the outcomes of 213 historic control patients with accelerated-phase CML who received treatment with interferon-alpha or with other modalities.
  • This may have implications in relation to subsequent therapy, because, according to the outcomes of patients who underwent allogeneic transplantation in accelerated phase at the authors' institution and from literature reports, the estimates of 5-year survival were 25-30%.
  • CONCLUSIONS: The current results suggest that imatinib improved survival compared with other therapies in patients with accelerated-phase CML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Anemia / chemically induced. Benzamides. Bone Marrow Transplantation. Cohort Studies. Cytogenetic Analysis. Female. Follow-Up Studies. Fusion Proteins, bcr-abl / analysis. Hemoglobins / analysis. Humans. Imatinib Mesylate. Interferon-alpha / therapeutic use. Longitudinal Studies. Male. Middle Aged. Remission Induction. Survival Rate. Treatment Outcome

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  • (PMID = 15830345.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Hemoglobins; 0 / Interferon-alpha; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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17. Zhou L, Wang AH, Wang L, You JH, Li JM, Shen ZX: [Efficacy and safety of imatinib in treatment of 151 chronic myeloid leukemia patients]. Zhonghua Xue Ye Xue Za Zhi; 2008 Jan;29(1):13-7
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  • [Title] [Efficacy and safety of imatinib in treatment of 151 chronic myeloid leukemia patients].
  • OBJECTIVE: To evaluate the safety and efficacy of imatinib in treatment of chronic myeloid leukemia (CML) patients.
  • RESULTS: One hundred and forty-two patients were evaluable with a median follow-up duration of 21.5 (6 -78) months. (1) The rate of cumulative complete hematologic response (CHR), major cytogenetic response (MCyR), complete cytogenetic response (CCyR) and complete molecular response (CMoR) in chronic phase (CP) CML patients were 96.9%, 82.6%, 76.1% and 29.4%, respectively.
  • These rates were significantly higher in patients with CP than in those with accelerated phase (AP) and blast crisis (BC) (P < 0.0001). (2) The overall survival (OS) rates at 1, 2 and 3 year were 100%, (97.3 +/- 1.9)% and (95.8 +/- 2.4)% for CP patients, they were (84.7 +/- 8.2)%, (77.0 +/- 10.4)% and (69.3 +/- 11.9)% for AP patients, and (62.9 +/- 8.9)%, (41.9 +/- 9.2)% and (28.5 +/- 9.1)% for BC patients, respectively (P < 0.0001).
  • Sokal score was also significantly associated with disease progression (P = 0.0467). (4) The adverse events of imatinib were moderate and tolerable.
  • CONCLUSIONS: Treatment of CML patients in CP with imatinib can induce high hematologic, cytogenetic and molecular response and overall survival, but can not do satisfactorily for patients in AP and BC.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use



18. 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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19. 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



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



21. Crawley C, Szydlo R, Lalancette M, Bacigalupo A, Lange A, Brune M, Juliusson G, Nagler A, Gratwohl A, Passweg J, Komarnicki M, Vitek A, Mayer J, Zander A, Sierra J, Rambaldi A, Ringden O, Niederwieser D, Apperley JF, Chronic Leukemia Working Party of the EBMT: Outcomes of reduced-intensity transplantation for chronic myeloid leukemia: an analysis of prognostic factors from the Chronic Leukemia Working Party of the EBMT. Blood; 2005 Nov 1;106(9):2969-76
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  • [Title] Outcomes of reduced-intensity transplantation for chronic myeloid leukemia: an analysis of prognostic factors from the Chronic Leukemia Working Party of the EBMT.
  • This study reports outcomes of allogeneic hematopoietic stem cell transplantation with reduced-intensity conditioning (RIC) in 186 patients with chronic myeloid leukemia (CML) from the European Group for Blood and Marrow Transplantation (EBMT).
  • The median age was 50 years, and 64% were in first chronic phase (CP1), CP2 13%, accelerated phase 17%, and blast crises 6%.
  • Acute graft-versus-host disease (GvHD) grade II to IV occurred in 32% and chronic GvHD in 43% (extensive in 24%).
  • ATG was associated with a lower incidence of chronic GvHD (cGvHD).
  • Adverse OS was associated with advanced disease (relative risk [RR], 3.4).
  • PFS was inferior in advanced disease (RR, 2.7) and a trend to improved outcomes with Fd/Bu/ATG (RR, 0.58).
  • RIC allografts are feasible in CML in first or second CP.
  • [MeSH-major] Bone Marrow Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Benzamides. Disease Progression. Europe. Female. Graft vs Host Disease. Humans. Imatinib Mesylate. Male. Middle Aged. Piperazines / therapeutic use. Prognosis. Pyrimidines / therapeutic use. Risk Factors. Societies, Scientific. Survival Rate. Transplantation Conditioning. Treatment Outcome



22. Tedeschi FA, Zalazar FE: HOXA9 gene expression in the chronic myeloid leukemia progression. Leuk Res; 2006 Nov;30(11):1453-6
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  • [Title] HOXA9 gene expression in the chronic myeloid leukemia progression.
  • In the present work we study the HOXA9 expression in sequential samples of patients with CML using RT-PCR.
  • The relative HOXA9 expression was higher in patients in the accelerated phase of the disease (p<0.005).
  • These first results could be considered as an evidence of an actual biological phenomenon that could provide additional information about the HOXA9 role in the CML progression.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Leukemic. Homeodomain Proteins / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Adult. Disease Progression. Fusion Proteins, bcr-abl / genetics. Humans. Middle Aged. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods



23. Stromskaya TP, Rybalkina EY, Kruglov SS, Zabotina TN, Mechetner EB, Turkina AG, Stavrovskaya AA: Role of P-glycoprotein in evolution of populations of chronic myeloid leukemia cells treated with imatinib. Biochemistry (Mosc); 2008 Jan;73(1):29-37
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  • [Title] Role of P-glycoprotein in evolution of populations of chronic myeloid leukemia cells treated with imatinib.
  • Imatinib mesylate (imatinib) is a new generation preparation that is now successfully used for treatment of cancer, particularly for chemotherapy of chronic myeloid leukemia (CML).
  • Imatinib inhibits the activity of chimeric kinase BCR-ABL, which is responsible for the development of CML.
  • The goal of this study was to investigate the role of a multidrug resistance protein, P-glycoprotein (Pgp), in the evolution of CML treated with imatinib.
  • We demonstrate here that although imatinib is a substrate for Pgp, cultured CML cells (strain K562/i-S9), overexpressing active Pgp, do not exhibit imatinib resistance.
  • Studies of CML patients in the accelerated phase have shown variations in the number of Pgp-positive cells (Pgp+) among individual patients treated with imatinib.
  • During treatment of patients with imatinib for 6-12 months, the number of Pgp-positive cells significantly increased in most patients.
  • We also compared the mode of Rh123 efflux by cells from CML patients who underwent imatinib treatment for 6-24 months and the responsiveness of patients to this therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. P-Glycoprotein / metabolism. Piperazines / therapeutic use. Pyrimidines / therapeutic use



24. 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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  • [Cites] Lancet. 2002 Feb 9;359(9305):487-91 [11853795.001]
  • [Cites] Blood. 2007 Dec 1;110(12):4005-11 [17785585.001]
  • [Cites] J Biol Chem. 2002 Aug 30;277(35):32214-9 [12077114.001]
  • [Cites] Cancer Cell. 2002 Aug;2(2):117-25 [12204532.001]
  • [Cites] Curr Opin Hematol. 2004 Jan;11(1):35-43 [14676625.001]
  • [Cites] Clin Cancer Res. 2005 May 1;11(9):3425-32 [15867244.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4500-5 [15930265.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2531-41 [16775234.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2542-51 [16775235.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1809-20 [16709930.001]
  • [Cites] Leukemia. 2006 Oct;20(10):1767-73 [16855631.001]
  • [Cites] Clin Cancer Res. 2006 Dec 15;12(24):7374-9 [17189410.001]
  • [Cites] Blood. 2007 Jan 15;109(2):500-2 [16990603.001]
  • [Cites] Haematologica. 2007 Sep;92(9):1238-41 [17768119.001]
  • [Cites] Leukemia. 2007 Oct;21(10):2204-6 [17541396.001]
  • [Cites] N Engl J Med. 2002 Feb 28;346(9):645-52 [11870241.001]
  • (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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25. Agis H, Krauth MT, Böhm A, Mosberger I, Müllauer L, Simonitsch-Klupp I, Walls AF, Horny HP, Valent P: Identification of basogranulin (BB1) as a novel immunohistochemical marker of basophils in normal bone marrow and patients with myeloproliferative disorders. Am J Clin Pathol; 2006 Feb;125(2):273-81
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  • In chronic myeloid leukemia (CML), basophilia is a diagnostic and prognostic variable.
  • We applied the antibasogranulin antibody BB1 on paraffin-embedded BM sections in 21 control samples (normal BM), 45 patients with CML, 9 with chronic idiopathic myelofibrosis, 11 with polycythemia vera, 19 with essential thrombocythemia, and 7 with indolent systemic mastocytosis.
  • BB1+ BM cells were found to be highly elevated in patients with CML compared with normal BM or other MPDs, with maximum counts found in accelerated phase CML (median, 160 cells/mm(2)).
  • In summary, BB1 (basogranulin) is a new immunohistochemical basophil marker that should allow quantification of basophils in CML at diagnosis and during therapy.
  • [MeSH-major] Basophils / chemistry. Bone Marrow / chemistry. DNA-Binding Proteins / analysis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood. Phosphoproteins / analysis. Transcription Factors / analysis

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  • (PMID = 16393678.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0500729
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / DNA-Binding Proteins; 0 / Phosphoproteins; 0 / Transcription Factors; 148814-46-4 / BNC1 protein, human
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26. Aguilera DG, Tsimberidou AM: Dasatinib in chronic myeloid leukemia: a review. Ther Clin Risk Manag; 2009 Apr;5(2):281-9
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  • [Title] Dasatinib in chronic myeloid leukemia: a review.
  • Deregulated BCR-ABL tyrosine kinase (TK) activity is the molecular marker for chronic myeloid leukemia (CML), which provides an identifiable target for developing therapeutic agents.
  • Imatinib mesylate, a BCR-ABL TK inhibitor, is the frontline therapy for CML.
  • In newly diagnosed patients with chronic phase CML, the rate of resistance to imatinib at 4 years was up to 20%, increasing to 70% to 90% for patients in the accelerated/blastic phase.
  • Dasatinib is well tolerated and has broad efficacy, resulting in durable responses in patients with any BCR-ABL mutation except for T3151 and mutations in codon 317 - most commonly F317L - including mutations that were highly resistant to imatinib, such as L248, Y253, E255, F359, and H396.
  • Dasatinib is recommended for CML in chronic, blastic or accelerated phase that is resistant or intolerant to imatinib.
  • Dasatinib was approved by the FDA at 100 mg once daily as the starting dose in patients with chronic phase CML and at 70 mg twice daily in patients with accelerated or blastic phase CML.
  • Other second-generation TKIs with activity in CML include nilotinib, bosutinib and INNO 406.
  • New molecules, such as the inhibitor of Aurora family serine-threonine kinases, MK0457, which has antileukemic activity in CML associated with a T315I mutation, are being investigated.

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  • [Cites] J Clin Oncol. 2009 Jan 20;27(3):469-71 [19075254.001]
  • [Cites] J Natl Cancer Inst. 2000 Oct 18;92(20):1641-50 [11036109.001]
  • [Cites] Haematologica. 2009 Jan;94(1):135-9 [19066329.001]
  • [Cites] Leukemia. 2008 Dec;22(12):2176-83 [18754032.001]
  • [Cites] Cancer Cell. 2008 Dec 9;14(6):485-93 [19061839.001]
  • [Cites] Cancer Res. 2008 Dec 1;68(23):9624-33 [19047139.001]
  • [Cites] J Hematol Oncol. 2008;1:15 [18828913.001]
  • [Cites] Blood. 2008 Aug 15;112(4):1005-12 [18477770.001]
  • [Cites] J Clin Oncol. 2008 Jul 1;26(19):3204-12 [18541900.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1200-6 [18401416.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2843-53 [18156496.001]
  • [Cites] Clin Cancer Res. 2008 Jan 15;14(2):352-9 [18223208.001]
  • [Cites] Cancer Chemother Pharmacol. 2008 Mar;61(3):365-76 [17429625.001]
  • [Cites] Blood. 2007 Dec 1;110(12):4055-63 [17720881.001]
  • [Cites] Lancet Oncol. 2007 Nov;8(11):1018-29 [17976612.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2309-15 [17496201.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5143-50 [17317857.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1267-75 [17519960.001]
  • [Cites] Blood. 2007 May 15;109(10):4143-50 [17264298.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3207-13 [17185463.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2303-9 [17138817.001]
  • [Cites] Blood. 2007 Jan 15;109(2):497-9 [16990591.001]
  • [Cites] J Clin Oncol. 2006 Nov 20;24(33):e51-2 [17114651.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1809-20 [16709930.001]
  • [Cites] Blood. 2006 Jul 1;108(1):28-37 [16522812.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2531-41 [16775234.001]
  • [Cites] Cancer Res. 2006 Jun 1;66(11):5790-7 [16740718.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4532-9 [16469872.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4100-9 [15867198.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4500-5 [15930265.001]
  • [Cites] J Med Chem. 2004 Dec 30;47(27):6658-61 [15615512.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3739-45 [15315971.001]
  • [Cites] N Engl J Med. 1999 Apr 29;340(17):1330-40 [10219069.001]
  • [Cites] Blood Cells Mol Dis. 1997 Dec;23(3):380-94 [9446752.001]
  • [Cites] Nat Med. 1996 May;2(5):561-6 [8616716.001]
  • [Cites] N Engl J Med. 1988 Oct 13;319(15):990-8 [3047582.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2940-2 [15251980.001]
  • [Cites] Science. 2004 Jul 16;305(5682):399-401 [15256671.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4010-22 [14982876.001]
  • [Cites] Mini Rev Med Chem. 2004 Mar;4(3):285-99 [15032675.001]
  • [Cites] Leukemia. 2004 Mar;18(3):401-8 [14724652.001]
  • [Cites] Oncogene. 2003 Oct 20;22(47):7389-95 [14576846.001]
  • [Cites] N Engl J Med. 2003 Oct 9;349(15):1451-64 [14534339.001]
  • [Cites] N Engl J Med. 2003 Mar 13;348(11):994-1004 [12637609.001]
  • [Cites] Leukemia. 2002 Nov;16(11):2190-6 [12399961.001]
  • [Cites] Clin Cancer Res. 2002 May;8(5):935-42 [12006504.001]
  • [Cites] Science. 2001 Aug 3;293(5531):876-80 [11423618.001]
  • [Cites] J Mol Diagn. 2009 Jan;11(1):4-11 [19095773.001]
  • (PMID = 19536317.001).
  • [ISSN] 1176-6336
  • [Journal-full-title] Therapeutics and clinical risk management
  • [ISO-abbreviation] Ther Clin Risk Manag
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2697539
  • [Keywords] NOTNLM ; BCR-ABL / chronic myeloid leukemia / dasatininb / tyrosine kinase inhibitor
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27. Rosti G, Castagnetti F, Gugliotta G, Palandri F, Martinelli G, Baccarani M: Dasatinib and nilotinib in imatinib-resistant Philadelphia-positive chronic myelogenous leukemia: a 'head-to-head comparison'. Leuk Lymphoma; 2010 Apr;51(4):583-91
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  • [Title] Dasatinib and nilotinib in imatinib-resistant Philadelphia-positive chronic myelogenous leukemia: a 'head-to-head comparison'.
  • Imatinib has revolutionized the treatment of patients with chronic myeloid leukemia (CML).
  • Dasatinib, approved in 2006 for the treatment of patients with CML in all phases who experience imatinib resistance or intolerance, has displayed significant efficacy, with a 2-year follow-up showing durable hematologic and cytogenetic responses, as well as prolonged progression-free and overall survival.
  • Nilotinib was approved in 2007 for the treatment of patients with CML in chronic phase or CML in accelerated phase, resistant or intolerant to prior therapy including imatinib, based on strong efficacy as well as a favorable safety profile.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use

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  • (PMID = 20302388.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
  • [Number-of-references] 30
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28. 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



29. Kim SH, Kim D, Kim DW, Goh HG, Jang SE, Lee J, Kim WS, Kweon IY, Park SH: Analysis of Bcr-Abl kinase domain mutations in Korean chronic myeloid leukaemia patients: poor clinical outcome of P-loop and T315I mutation is disease phase dependent. Hematol Oncol; 2009 Dec;27(4):190-7
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  • [Title] Analysis of Bcr-Abl kinase domain mutations in Korean chronic myeloid leukaemia patients: poor clinical outcome of P-loop and T315I mutation is disease phase dependent.
  • Despite durable responses to imatinib in chronic myeloid leukaemia (CML), mutations in Bcr-Abl kinase domain (KD) are known to induce imatinib resistance and cause poor clinical outcome.
  • We characterized Bcr-Abl KD mutations in 137 Korean CML patients with imatinib resistance (n = 111) or intolerance (n = 26) using allele specific oligonucleotide polymerase chain reaction (PCR) and direct sequencing.
  • Seventy (51%) patients harboured 81 mutations of 20 different types with increasing prevalence in advanced phase.
  • T315I was the most common mutation and P-loop was the hottest spot in Bcr-Abl KD.
  • Survival analysis according to disease phase of mutation being detected and type of mutations provided correlation between P-loop or T315I mutation and poor overall survival in blast crisis, but not in accelerated phase (AP) or chronic phase (CP), indicating poor clinical outcome of particular mutations depends on disease phase.
  • CML patients with imatinib resistance showed high rate (63%) of mutations in Bcr-Abl KD and therefore CML patients who do not respond to imatinib should be the candidates for mutation screening as molecular monitoring.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Piperazines / pharmacology. Pyrimidines / pharmacology
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / pharmacology. Benzamides. DNA Mutational Analysis. Disease Progression. Drug Resistance, Neoplasm. Female. Humans. Imatinib Mesylate. Korea / epidemiology. Male. Middle Aged. Prognosis. Protein Kinase Inhibitors / pharmacology. Protein Structure, Tertiary. Survival Rate. Treatment Outcome. Young Adult

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  • [Copyright] Copyright (c) 2009 John Wiley & Sons, Ltd.
  • (PMID = 19274615.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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30. Liu Q, Zhu Y, Qiu HX, Qiu HR, Wang R, Xu W, Li JY: [Analysis of chromosome-8 aberrations in myeloid malignancies with complex chromosome abnormalities]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Oct;16(5):993-6
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  • [Title] [Analysis of chromosome-8 aberrations in myeloid malignancies with complex chromosome abnormalities].
  • To investigate the chromosome-8 aberrations in myeloid malignancies with complex chromosome abnormalities (CCAs), 81 cases of myeloid malignancies with CCAs were analysed by conventional chromosome analysis and multiplex fluorescence in situ hybridization.
  • The 81 cases included 25 cases of acute myeloid leukemia (AML), 35 cases of chronic myeloid leukemia (CML) and 21 cases of myelodysplastic syndrome (MDS).
  • The results showed that all chromosomes were involved in CCAs, and the incidence of chromosome-8 abnormality was 35.8% (29 out of 81 cases) in myeloid malignancies with CCAs, which in AML, CML and MDS patients were 56% (14/25), 28.6% (10/35) and 23.81% (5/21), respectively.
  • In CML, the incidences of accelerated phase and blast phase were 20% (1/5) and 33.3% (9/27), respectively.
  • In conclusion, aberrations of chromosome 8 were common in myeloid malignancies with CCAs, and may be related to progression of the disease.

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  • (PMID = 18928581.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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31. 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



32. Rao S, Sen R, Singh S, Ghalaut PS, Arora BB: Grading of marrow fibrosis in chronic myeloid leukemia--a comprehensive approach. Indian J Pathol Microbiol; 2005 Jul;48(3):341-4
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  • [Title] Grading of marrow fibrosis in chronic myeloid leukemia--a comprehensive approach.
  • In the course of Chronic myeloid leukemia (CML), appearance of increased number of blasts may herald evolution of accelerated phase as well as onset of marrow fibrosis (MF) thereby necessitating the need to perform trephine biopsy for correct diagnosis and appropriate treatment.
  • We performed 50 bone marrow (BM) trephine biopsies in patients of CML in order to assess the incidence and degree of MF.
  • A positive correlation was found between increasing grades of MF and number of megakaryocytes in the BM.
  • [MeSH-major] Bone Marrow Cells / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Primary Myelofibrosis / pathology



33. Cavalcanti GB Jr, Scheiner MA, Simões Magluta EP, Vasconcelos FC, Klumb CE, Maia RC: p53 flow cytometry evaluation in leukemias: correlation to factors affecting clinical outcome. Cytometry B Clin Cytom; 2010 Jul;78(4):253-9
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  • p53 is a cell cycle checkpoint control protein that assesses DNA damage and acts as a transcription factor regulating genes, which control cell growth, DNA repair, and apoptosis. p53 mutations have been found in a wide variety of different cancers including flow cytometric assessment of p53 protein expression using anti-p53 monoclonal antibodies.
  • We studied p53 protein expression by flow cytometry (FC) assay in 223 blood and/or bone marrow samples from 72 patients with chronic myeloid leukemia (CML): 54 in chronic phase (CML-CP), 7 in accelerated phase (CML-AP), and 11 in blastic phase (CML-BP); 64 patients with chronic lymphoid leukemia (CLL): (34 at diagnosis, 21 in previously treated, and 9 with Richter's syndrome); 44 patients with acute lymphoid leukemia (ALL): 36 at diagnosis and 8 in relapse; and 43 acute myeloid leukemia (AML): 27 de novo, 7 in relapse, and 9 secondary. p53 protein expression was observed in 64 of 223 patient's samples: 14/64 (21.9%) CLL, 13/44 (29.5%) ALL, 19/43 (44.2%) AML, and 17/72 (23.6%) CML.
  • Highest levels were detected in the advanced phases of CLL, ALL, and CML.
  • In addition, in patients with AML, high levels of p53 expression were detected in secondary and relapse disease and also in de novo AML cases.
  • Our results demonstrated that p53 expression levels are strongly associated with advanced disease.
  • [MeSH-major] Flow Cytometry / methods. Leukemia / metabolism. Leukemia / therapy. Tumor Suppressor Protein p53 / metabolism

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  • [Copyright] (c) 2010 Clinical Cytometry Society.
  • (PMID = 20198607.001).
  • [ISSN] 1552-4957
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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34. Olsson-Strömberg U, Hermansson M, Lundán T, Ohm AC, Engdahl I, Höglund M, Simonsson B, Porkka K, Barbany G: Molecular monitoring and mutation analysis of patients with advanced phase CML and Ph+ ALL receiving dasatinib. Eur J Haematol; 2010 Nov;85(5):399-404
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  • [Title] Molecular monitoring and mutation analysis of patients with advanced phase CML and Ph+ ALL receiving dasatinib.
  • As a result of the excellent responses achieved in chronic phase chronic myeloid leukemia since the introduction of imatinib, sensitive techniques such as reverse transcriptase real-time PCR are warranted to monitor patients receiving tyrosine kinase inhibitors (TKI).
  • Our objective was to determine the value of molecular monitoring Ph-positive leukemias under dasatinib treatment.
  • We used real-time PCR and ABL1 kinase domain sequencing on sequential samples from 11 patients with Philadelphia-positive leukemias who received dasatinib.
  • We were able to detect pre-existing mutations in the kinase domain of BCR-ABL1 in four patients, particularly in patients with high BCR-ABL1 transcript levels.
  • We conclude that sensitive molecular monitoring with real-time PCR for BCR-ABL1 transcripts and mutation screening of the ABL1 kinase domain of patients with Philadelphia-positive leukemias are valuable for patient management, however, mutation findings should be interpreted with caution, as mutant clones not always behave in vivo as predicted by in vitro assays.
  • [MeSH-major] DNA Mutational Analysis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid, Accelerated Phase / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Clone Cells / pathology. Dasatinib. Female. Fusion Proteins, bcr-abl / genetics. Humans. Male. Middle Aged. Polymerase Chain Reaction / methods. RNA, Neoplasm / genetics. Young Adult

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  • [Copyright] © 2010 John Wiley & Sons A/S.
  • (PMID = 20659155.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Pyrimidines; 0 / RNA, Neoplasm; 0 / Thiazoles; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
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35. Kerbauy FR, Storb R, Hegenbart U, Gooley T, Shizuru J, Al-Ali HK, Radich JP, Maloney DG, Agura E, Bruno B, Epner EM, Chauncey TR, Blume KG, Niederwieser D, Sandmaier BM: Hematopoietic cell transplantation from HLA-identical sibling donors after low-dose radiation-based conditioning for treatment of CML. Leukemia; 2005 Jun;19(6):990-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hematopoietic cell transplantation from HLA-identical sibling donors after low-dose radiation-based conditioning for treatment of CML.
  • A total of 24 patients (median age 58; range, 27-71 years) with chronic myeloid leukemia (CML) in first chronic (CP1) (n=14), second chronic (n=4), or accelerated phase (n=6) who were not candidates for conventional hematopoietic cell transplantation (HCT), received nonmyeloablative HCT from HLA-matched siblings a median of 28.5 (range, 11-271) months after diagnosis.
  • The 2-year estimate of chronic GVHD was 32%.
  • This study shows encouraging remission rates for patients with CML not eligible for conventional allografting.

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  • (PMID = 15800667.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA18029; United States / NCI NIH HHS / CA / CA78902; United States / NCI NIH HHS / CA / CA49605; United States / NCI NIH HHS / CA / CA15704; United States / NCI NIH HHS / CA / P01 CA078902
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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36. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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37. 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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38. Ahmad R, Tripathi AK, Tripathi P, Singh S, Singh R, Singh RK: Malondialdehyde and protein carbonyl as biomarkers for oxidative stress and disease progression in patients with chronic myeloid leukemia. In Vivo; 2008 Jul-Aug;22(4):525-8
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  • [Title] Malondialdehyde and protein carbonyl as biomarkers for oxidative stress and disease progression in patients with chronic myeloid leukemia.
  • However, evidence for this association has often been lacking because of a lack of specific biomarkers and methods available to evaluate oxidative stress status in humans with disease conditions.
  • The aim of this study was to investigate the plasma levels of malondialdehyde (MDA) and protein carbonyl (PC) as biomarkers for oxidative stress and disease progression in patients with chronic myeloid leukemia (CML).
  • MATERIALS AND METHODS: The study included 20 CML patients and 10 age-and sex-matched healthy control volunteers.
  • The mean age of CML patients was 37.11+/-11.36 years and that of controls was 31.07+/-7.60 years.
  • RESULTS: There was a significant increase (p<0.05) in plasma MDA and PC levels in CML patients as compared to healthy volunteers.
  • Our results also showed that plasma MDA and PC levels were significantly higher (p<0.001) in both chronic phase (CML-CP) and accelerated phase (CML-AP) as compared to healthy volunteers.
  • During the follow-up of 12 months, two patients of CML-CP progressed to the accelerated phase.
  • The mean plasma levels of MDA and PC in patients with CML-CP who progressed to CML-AP were found to be higher than in patients with CML-CP who did not progress to the accelerated phase.
  • CONCLUSION: Plasma MDA and PC appears to reflect the oxidative stress status and disease progression in CML and can be used as biomarkers for oxidative stress and disease progression.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myeloid, Accelerated Phase / metabolism. Leukemia, Myeloid, Chronic-Phase / metabolism. Malondialdehyde / metabolism. Oxidative Stress. Protein Carbonylation. Proteins / metabolism
  • [MeSH-minor] Adult. Case-Control Studies. Disease Progression. Humans. Time Factors



39. Quintás-Cardama A, Kim TD, Cataldo V, le Coutre P: Nilotinib. Recent Results Cancer Res; 2010;184:103-17
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Therapy with imatinib mesylate is a standard of care for most patients with Philadelphia chromosome-positive chronic myeloid leukemia (CML).
  • However, resistance or intolerance to imatinib develops in a considerable number of patients leading to relapse or discontinuation of treatment.
  • Nilotinib is a rationally designed second-generation tyrosine kinase inhibitor (TKI) with improved affinity and specificity against the BCR-ABL kinase, when compared with imatinib.
  • Considerable efficacy after imatinib failure has been demonstrated in clinical trials leading to nilotinib's current approval as second-line therapy for CML in chronic and accelerated phase (AP).
  • The role of nilotinib as first-line treatment for CML, in combinatorial strategies and in the context of specific BCR-ABL mutations, requires future studies.

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  • (PMID = 20072834.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Pyrimidines
  • [Number-of-references] 62
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40. Zhu Y, Li JY, Xu W, Qiu HR, Chen LJ, Pan JL, Shen YF, Xue YQ: [Multiplex fluorescence in situ hybridization for detecting complex chromosomal aberrations in chronic myeloid leukemia in blast crisis]. Zhonghua Xue Ye Xue Za Zhi; 2007 Jul;28(7):458-61
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  • [Title] [Multiplex fluorescence in situ hybridization for detecting complex chromosomal aberrations in chronic myeloid leukemia in blast crisis].
  • OBJECTIVE: To investigate the value of multiplex fluorescence in situ hybridization (M-FISH) for the detection of complex chromosomal abnormalities (CCA) of chronic myeloid leukemia in blast crisis (CML-BC).
  • METHODS: M-FISH was used to study 26 cases of CML-BC with CCA assayed by conventional cytogenetics (CC).
  • All chromosomes were involved in CML-BC, and chromosomes 17, 2, 8, 16 involvements were the most frequent.
  • CONCLUSIONS: M-FISH can refine CCA in CML-BC, find out or correct the missed or misidentified abnormalities by CC.
  • The frequent secondary chromosomal abnormalities in CML-BC with CCA are different from that in CML.
  • [MeSH-major] Blast Crisis / genetics. Chromosome Aberrations. In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Accelerated Phase / genetics

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  • (PMID = 18072628.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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41. Lange T, Park B, Willis SG, Deininger MW: BCR-ABL kinase domain mutations in chronic myeloid leukemia: not quite enough to cause resistance to imatinib therapy? Cell Cycle; 2005 Dec;4(12):1761-6
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  • [Title] BCR-ABL kinase domain mutations in chronic myeloid leukemia: not quite enough to cause resistance to imatinib therapy?
  • Patients with chronic myeloid leukemia (CML) treated with imatinib in early chronic phase tend to have durable remissions, but there is a high rate of relapse in patients with advanced disease.
  • Mutations in the kinase domain of BCR-ABL that impair drug binding have been identified as the major mechanism of resistance.
  • In the present study we have used a highly sensitive PCR assay to screen for kinase domain mutations in pretherapeutic samples from CML patients, irrespective of their subsequent response to imatinib.
  • We find that kinase domain mutations are demonstrable in approximately 1/3 of patients with accelerated phase or blast crisis and that the presence of two copies of the Philadelphia chromosome is strongly correlated with mutation detection.
  • Unexpectedly, kinase domain mutant clones were not invariably selected in the presence of drug, suggesting that additional mechanisms must contribute to a fully drug resistant leukemia.
  • [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. Mutation / genetics. Phosphotransferases / genetics. Piperazines / pharmacology. Pyrimidines / pharmacology



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



43. Oehler VG, Yeung KY, Choi YE, Bumgarner RE, Raftery AE, Radich JP: The derivation of diagnostic markers of chronic myeloid leukemia progression from microarray data. Blood; 2009 Oct 8;114(15):3292-8
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  • [Title] The derivation of diagnostic markers of chronic myeloid leukemia progression from microarray data.
  • Currently, limited molecular markers exist that can determine where in the spectrum of chronic myeloid leukemia (CML) progression an individual patient falls at diagnosis.
  • Gene expression profiles can predict disease and prognosis, but most widely used microarray analytical methods yield lengthy gene candidate lists that are difficult to apply clinically.
  • Consequently, we applied a probabilistic method called Bayesian model averaging (BMA) to a large CML microarray dataset.
  • BMA identified 6 genes (NOB1, DDX47, IGSF2, LTB4R, SCARB1, and SLC25A3) that discriminated chronic phase (CP) from blast crisis (BC) CML.
  • In CML, phase labels divide disease progression into discrete states.
  • In validation studies of 88 patients, the 6-gene signature discriminated early CP from late CP, accelerated phase, and BC.
  • This distinction between early and late CP is not possible with current classifications, which are based on known duration of disease.
  • Because therapeutic outcomes are so closely tied to disease phase, these probabilities can be used to determine a risk-based treatment strategy at diagnosis.

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  • [Cites] Blood. 2006 Mar 15;107(6):2507-16 [16293596.001]
  • [Cites] Leukemia. 2006 Jan;20(1):61-7 [16270044.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 21;103(8):2794-9 [16477019.001]
  • [Cites] N Engl J Med. 2006 Dec 7;355(23):2408-17 [17151364.001]
  • [Cites] Leukemia. 2007 Jan;21(1):93-101 [17109025.001]
  • [Cites] BMC Genomics. 2007;8:385 [17956600.001]
  • [Cites] Clin Cancer Res. 2008 Feb 15;14(4):1065-72 [18258665.001]
  • [Cites] Nucleic Acids Res. 2008 Apr;36(7):e43 [18346969.001]
  • [Cites] Genome Biol. 2008;9(7):R118 [18652698.001]
  • [Cites] Blood. 2000 Nov 15;96(10):3343-56 [11071626.001]
  • [Cites] N Engl J Med. 2001 Feb 22;344(8):539-48 [11207349.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1031-7 [11287972.001]
  • [Cites] Nat Biotechnol. 2001 Apr;19(4):342-7 [11283592.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1701-7 [11535500.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):15149-54 [11742071.001]
  • [Cites] Nat Med. 2002 Jan;8(1):68-74 [11786909.001]
  • [Cites] Blood. 2002 May 1;99(9):3472-5 [11964322.001]
  • [Cites] Blood. 2002 May 15;99(10):3530-9 [11986204.001]
  • [Cites] Nat Genet. 2002 Dec;32 Suppl:547-51 [12454652.001]
  • [Cites] Nat Rev Cancer. 2003 Apr;3(4):267-75 [12671665.001]
  • [Cites] Genomics. 2003 Jun;81(6):618-22 [12782131.001]
  • [Cites] Pflugers Arch. 2004 Feb;447(5):689-709 [14598172.001]
  • [Cites] Cancer Res. 2004 Feb 15;64(4):1515-21 [14973113.001]
  • [Cites] Ann N Y Acad Sci. 2004 Jun;1022:9-16 [15251933.001]
  • [Cites] Bone Marrow Transplant. 1996 May;17 Suppl 3:S49-54 [8769702.001]
  • [Cites] Br J Haematol. 1997 Apr;97(1):76-85 [9136944.001]
  • [Cites] N Engl J Med. 1999 Jul 15;341(3):164-72 [10403855.001]
  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Bioinformatics. 2005 May 15;21(10):2394-402 [15713736.001]
  • [Cites] Blood. 2006 Jan 1;107(1):205-12 [16144796.001]
  • [Cites] Haematologica. 2006 Feb;91(2):152 [16461297.001]
  • (PMID = 19654405.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD054511; United States / NCI NIH HHS / CA / K25 CA106988-05; United States / NIAID NIH HHS / AI / U54 AI057141; United States / NCI NIH HHS / CA / CA18029; United States / NHLBI NIH HHS / HL / P50HL073996; United States / NCI NIH HHS / CA / R01 CA140371; United States / NCRR NIH HHS / RR / R24 RR021863; United States / NCI NIH HHS / CA / K25CA106988; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCRR NIH HHS / RR / R24RR021863-01A1; United States / NIGMS NIH HHS / GM / R01 GM084163-01A1; United States / PHS HHS / / R01HDO54511-01A1; United States / NIGMS NIH HHS / GM / GM084163-01A1; United States / NIGMS NIH HHS / GM / R01 GM084163; United States / NIDCR NIH HHS / DE / R01DE012212-06; United States / NHLBI NIH HHS / HL / P50 HL073996; United States / NIAID NIH HHS / AI / U54AI057141; United States / NIGMS NIH HHS / GM / R01 GM084163-02; None / None / / K25 CA106988-05; United States / NCRR NIH HHS / RR / UL1 RR025014; None / None / / R01 GM084163-02; United States / NIDCR NIH HHS / DE / R01 DE012212; United States / NCRR NIH HHS / RR / UL1RR025014-01; United States / NIGMS NIH HHS / GM / R01GM084163-01A1; United States / NICHD NIH HHS / HD / R24 HD042828; United States / NCI NIH HHS / CA / K25 CA106988
  • [Publication-type] Clinical Trial; 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 / Biomarkers, Tumor; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC2759651
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44. Kantarjian H, Giles F, Wunderle L, Bhalla K, O'Brien S, Wassmann B, Tanaka C, Manley P, Rae P, Mietlowski W, Bochinski K, Hochhaus A, Griffin JD, Hoelzer D, Albitar M, Dugan M, Cortes J, Alland L, Ottmann OG: Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL. N Engl J Med; 2006 Jun 15;354(24):2542-51
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  • [Title] Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL.
  • BACKGROUND: Resistance to imatinib mesylate can occur in chronic myelogenous leukemia (CML).
  • Preclinical in vitro studies have shown that nilotinib (AMN107), a new BCR-ABL tyrosine kinase inhibitor, is more potent than imatinib against CML cells by a factor of 20 to 50.
  • METHODS: In a phase 1 dose-escalation study, we assigned 119 patients with imatinib-resistant CML or acute lymphoblastic leukemia (ALL) to receive nilotinib orally at doses of 50 mg, 100 mg, 200 mg, 400 mg, 600 mg, 800 mg, and 1200 mg once daily and at 400 mg and 600 mg twice daily.
  • Of 33 patients with the blastic phase of disease, 13 had a hematologic response and 9 had a cytogenetic response; of 46 patients with the accelerated phase, 33 had a hematologic response and 22 had a cytogenetic response; 11 of 12 patients with the chronic phase had a complete hematologic remission.
  • CONCLUSIONS: Nilotinib has a relatively favorable safety profile and is active in imatinib-resistant CML. (ClinicalTrials.gov number, NCT00109707 [ClinicalTrials.gov].).
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Fusion Proteins, bcr-abl / antagonists & inhibitors. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage

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  • [Copyright] Copyright 2006 Massachusetts Medical Society.
  • [CommentIn] N Engl J Med. 2006 Jun 15;354(24):2594-6 [16775240.001]
  • (PMID = 16775235.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00109707
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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45. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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46. Chen Y, Peng C, Li D, Li S: Molecular and cellular bases of chronic myeloid leukemia. Protein Cell; 2010 Feb;1(2):124-32
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  • [Title] Molecular and cellular bases of chronic myeloid leukemia.
  • Chronic myeloid leukemia (CML) is a myeloproliferative disease characterized by the overproduction of granulocytes, which leads to high white blood cell counts and splenomegaly in patients.
  • Based on clinical symptoms and laboratory findings, CML is classified into three clinical phases, often starting with a chronic phase, progressing to an accelerated phase and ultimately ending in a terminal phase called blast crisis.
  • Blast crisis phase of CML is clinically similar to an acute leukemia; in particular, B-cell acute lymphoblastic leukemia (B-ALL) is a severe form of acute leukemia in blast crisis, and there is no effective therapy for it yet.
  • CML is induced by the BCR-ABL oncogene, whose gene product is a BCR-ABL tyrosine kinase.
  • Currently, inhibition of BCR-ABL kinase activity by its kinase inhibitor such as imatinib mesylate (Gleevec) is a major therapeutic strategy for CML.
  • However, the inability of BCR-ABL kinase inhibitors to completely kill leukemia stem cells (LSCs) indicates that these kinase inhibitors are unlikely to cure CML.
  • In addition, drug resistance due to the development of BCRABL mutations occurs before and during treatment of CML with kinase inhibitors.
  • In this review, we will focus on LSCs in CML by summarizing and discussing available experimental results, including the original studies from our own laboratory.
  • [MeSH-major] Fusion Proteins, bcr-abl / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Neoplastic Stem Cells / enzymology. Neoplastic Stem Cells / pathology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] 5-Lipoxygenase-Activating Proteins / metabolism. Animals. Benzamides. Disease Models, Animal. Humans. Imatinib Mesylate. Male. Mice. PTEN Phosphohydrolase / metabolism. Philadelphia Chromosome. Piperazines / therapeutic use. Point Mutation. Protein Structure, Tertiary. Pyrimidines / therapeutic use

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  • (PMID = 21203982.001).
  • [ISSN] 1674-8018
  • [Journal-full-title] Protein & cell
  • [ISO-abbreviation] Protein Cell
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 5-Lipoxygenase-Activating Proteins; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC4875160
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47. 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



48. Singh RK, Tripathi AK, Tripathi P, Singh S, Singh R, Ahmad R: Studies on biomarkers for oxidative stress in patients with chronic myeloid leukemia. Hematol Oncol Stem Cell Ther; 2009;2(1):285-8
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  • [Title] Studies on biomarkers for oxidative stress in patients with chronic myeloid leukemia.
  • BACKGROUND: Chronic myeloid leukemia (CML) is a myeloproliferative disorder with a unique genetic rearrangement, the Philadelphia chromosome.
  • The aim of this study was to evaluate the products of protein oxidation and lipid peroxidation in plasma as biomarkers of oxidative stress in CML patients.
  • PATIENTS AND METHODS: The study included 40 CML patients and 20 age- and sex-matched healthy volunteers.
  • Of 40 CML patients, 28 were in chronic phase (CML-CP) and 12 in accelerated phase (CML-AP).
  • RESULTS: There were significant differences (P < .05) in plasma levels of PC, TBARS and LOOH in CML, CML-CP and CML-AP patients as compared to controls.
  • CONCLUSION: PC, TBARS and LOOH might reflect oxidative stress in CML patients and might be used as biomarkers in such patients.
  • [MeSH-major] Biomarkers, Tumor / analysis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Oxidative Stress / physiology



49. Quintás-Cardama A, Kantarjian H, Ravandi F, O'Brien S, Thomas D, Vidal-Senmache G, Wierda W, Kornblau S, Cortes J: Bleeding diathesis in patients with chronic myelogenous leukemia receiving dasatinib therapy. Cancer; 2009 Jun 1;115(11):2482-90
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  • [Title] Bleeding diathesis in patients with chronic myelogenous leukemia receiving dasatinib therapy.
  • BACKGROUND: The most frequent nonhematologic side effects associated with dasatinib therapy in patients with chronic myeloid leukemia (CML) are gastrointestinal, rash, and fluid retention syndromes.
  • In the current study, the authors investigated the risk factors and management of bleeding associated with dasatinib therapy for CML after imatinib failure.
  • METHODS: The bleeding episodes associated with dasatinib therapy in 138 patients with CML who were consecutively treated at the study institution in clinical trials were evaluated.
  • RESULTS: Bleeding occurred in 32 (23%) patients (grade >or=3 in 9 [7%] patients [according to National Cancer Institute Common Toxicity Criteria]), including in 12% of patients treated in chronic phase, 31% of patients treated in accelerated phase (AP), and 35% of patients treated in blast phase (BP) (P = .02).
  • Although 37% of episodes occurred with platelet counts >100 x 10(9)/L, multivariate analysis identified thrombocytopenia and advanced phase CML as risk factors for bleeding.
  • CONCLUSIONS: Bleeding occurs during dasatinib therapy, particularly in patients with AP or BP disease and low platelet counts.
  • [MeSH-major] Hemorrhagic Disorders / chemically induced. Leukemia, Myeloid, Chronic-Phase / complications. Leukemia, Myeloid, Chronic-Phase / drug therapy. Pyrimidines / adverse effects. Thiazoles / adverse effects

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  • [Copyright] (c) 2009 American Cancer Society.
  • [Cites] Science. 2000 Sep 15;289(5486):1938-42 [10988075.001]
  • [Cites] J Natl Cancer Inst. 2008 Jul 2;100(13):926-39 [18577747.001]
  • [Cites] N Engl J Med. 2002 Feb 28;346(9):645-52 [11870241.001]
  • [Cites] Blood. 2003 Jan 15;101(2):690-8 [12509383.001]
  • [Cites] N Engl J Med. 2003 Mar 13;348(11):994-1004 [12637609.001]
  • [Cites] Cancer Res. 2004 Jan 15;64(2):672-7 [14744784.001]
  • [Cites] Science. 2004 Jul 16;305(5682):399-401 [15256671.001]
  • [Cites] J Biol Chem. 2004 Aug 13;279(33):34227-39 [15175350.001]
  • [Cites] Science. 1997 Jul 11;277(5323):242-5 [9211853.001]
  • [Cites] Development. 1999 Jun;126(14):3047-55 [10375497.001]
  • [Cites] J Med Chem. 2004 Dec 30;47(27):6658-61 [15615512.001]
  • [Cites] Mol Pharmacol. 2006 May;69(5):1527-33 [16436588.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2531-41 [16775234.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3207-13 [17185463.001]
  • [Cites] Drug Metab Dispos. 2008 Jul;36(7):1357-64 [18420784.001]
  • [Cites] J Clin Oncol. 2008 Jul 1;26(19):3204-12 [18541900.001]
  • [Cites] Blood. 2001 Apr 1;97(7):1990-8 [11264163.001]
  • (PMID = 19280591.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ NIHMS629436; NLM/ PMC4180711
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50. Hazarika M, Jiang X, Liu Q, Lee SL, Ramchandani R, Garnett C, Orr MS, Sridhara R, Booth B, Leighton JK, Timmer W, Harapanhalli R, Dagher R, Justice R, Pazdur R: Tasigna for chronic and accelerated phase Philadelphia chromosome--positive chronic myelogenous leukemia resistant to or intolerant of imatinib. Clin Cancer Res; 2008 Sep 1;14(17):5325-31
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  • [Title] Tasigna for chronic and accelerated phase Philadelphia chromosome--positive chronic myelogenous leukemia resistant to or intolerant of imatinib.
  • PURPOSE: This Food and Drug Administration (FDA) approval report describes the data and analyses leading to the approval by the FDA of nilotinib (Tasigna, AMN-107; Novartis Pharmaceuticals Corporation), an inhibitor of Bcr-Abl tyrosine kinase, for the treatment of chronic-phase (CP) and accelerated-phase (AP) chronic myelogenous leukemia (CML) resistant to or intolerant of imatinib.
  • EXPERIMENTAL DESIGN: The FDA approval of the efficacy and safety of nilotinib was based on the results of an ongoing single-arm, open-label, phase 2 clinical trial.
  • The primary end point for CML-CP was unconfirmed major cytogenetic response.
  • The efficacy end point for CML-AP was confirmed hematologic response.
  • The median duration of response has not been reached for both CML-CP and CML-AP responding patients.
  • In CML-CP patients, the common serious drug-related adverse reactions were thrombocytopenia and neutropenia.
  • In CML-AP patients, the common serious drug-related adverse reactions were thrombocytopenia, neutropenia, pneumonia, febrile neutropenia, leukopenia, intracranial hemorrhage, elevated lipase, and pyrexia.
  • Nilotinib prolongs the QT interval and sudden deaths have been reported; these risks and appropriate risk minimization strategies are described in a boxed warning on the labeling.
  • FDA granted accelerated approval to nilotinib (Tasigna) for use in the treatment of CP and AP Philadelphia chromosome positive CML in adult patients resistant to or intolerant of prior therapy that included imatinib.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Benzamides. Clinical Trials, Phase II as Topic. Drug Approval. Drug Resistance, Neoplasm. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Protein Kinase Inhibitors / therapeutic use. United States. United States Food and Drug Administration

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  • (PMID = 18765523.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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51. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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52. Vasconcelos FC, Gattass CR, Rumjanek VM, Maia RC: Pomolic acid-induced apoptosis in cells from patients with chronic myeloid leukemia exhibiting different drug resistance profile. Invest New Drugs; 2007 Dec;25(6):525-33
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  • [Title] Pomolic acid-induced apoptosis in cells from patients with chronic myeloid leukemia exhibiting different drug resistance profile.
  • Pomolic acid (PA) is a pentacyclic triterpene which has been previously described as active in inhibiting the growth of K562 cell line-originated from chronic myeloid leukemia (CML) in blast crisis-and its vincristine-resistant derivative K562-Lucena1.
  • In this work, cells from CML patients were treated with PA and the apoptotic index was compared with the multidrug resistance (MDR) profile and clinical status of the patients.
  • Our findings show that PA 12.5 microg/ml at 24 h (p = 0.000), at 48 h (p = 0.012) and at 72 h (p = 0.005) has a potent apoptotic index in CML cells as compared to mononuclear cells from healthy donors.
  • PA was capable to induce apoptosis in cells from CML patients exhibiting functional MDR phenotype but not in P-glycoprotein expression.
  • In addition, PA was effective in chronic as well as in blast phase of CML.
  • These results suggest that PA may be an effective agent for the treatment of CML.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Drug Resistance, Neoplasm. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Oleanolic Acid / analogs & derivatives
  • [MeSH-minor] Blast Crisis / drug therapy. Blast Crisis / pathology. Drug Resistance, Multiple. Humans. Leukemia, Myeloid, Accelerated Phase / drug therapy. Leukemia, Myeloid, Accelerated Phase / pathology. Leukemia, Myeloid, Chronic-Phase / drug therapy. Leukemia, Myeloid, Chronic-Phase / pathology



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

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  • (PMID = 19254884.001).
  • [ISSN] 1557-9190
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
  • [Number-of-references] 51
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54. Martin MG, Dipersio JF, Uy GL: Management of the advanced phases of chronic myelogenous leukemia in the era of tyrosine kinase inhibitors. Leuk Lymphoma; 2009 Jan;50(1):14-23
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  • [Title] Management of the advanced phases of chronic myelogenous leukemia in the era of tyrosine kinase inhibitors.
  • Imatinib has revolutionised the management of chronic phase chronic myelogenous leukemia (CML).
  • Unfortunately it has had less of an impact on the management of the advanced phases of CML.
  • These historically difficult-to-treat phases of disease remain largely resistant to therapy.
  • Even when responses are obtained with the tyrosine kinase inhibitors, they are brief, particularly in blast phase (BP) disease.
  • But transplant outcomes are dependent on cytogenetic and gross disease burden at the time of transplant.
  • This review will compare and contrast the various tyrosine kinase- and non-tyrosine kinase inhibitor-based treatments for accelerated and BP CML before allogeneic transplantation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors

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  • (PMID = 19117213.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 80
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55. Basak G, Torosian T, Snarski E, Niesiobedzka J, Majewski M, Gronkowska A, Urbanowska E, Jedrzejczak W: Hematopoietic stem cell transplantation for T315I-mutated chronic myelogenous leukemia. Ann Transplant; 2010 Apr-Jun;15(2):68-70
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  • [Title] Hematopoietic stem cell transplantation for T315I-mutated chronic myelogenous leukemia.
  • BACKGROUND: The T315I mutation of BCR/ABL gene is known to produce complete resistance of chronic myelogenous leukemia (CML) to all currently available BCR/ABL inhibitors.
  • However, evidence on efficiency of this treatment modality in CML with T315I mutation is lacking.
  • CASE REPORT: A 25-year-old patient was diagnosed with Philadelphia chromosome positive CML in accelerated phase.
  • Moreover, despite escalation of imatinib dosage, the disease relapsed after further 3 months of treatment.
  • Molecular studies revealed T315I mutation of BCR/ABL gene.
  • The course of transplantation was complicated by staphylococcal sepsis, grade I skin acute GvHD and limited chronic skin GVHD.
  • CONCLUSIONS: The clinical course of this case supports the idea that allogeneic hematopoietic transplantation is a viable treatment option for patients with CML bearing T315I mutation.
  • [MeSH-major] Genes, abl. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Mutation, Missense
  • [MeSH-minor] Adult. Amino Acid Substitution. Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / genetics. Humans. Leukemia, Myeloid, Accelerated Phase / drug therapy. Leukemia, Myeloid, Accelerated Phase / genetics. Leukemia, Myeloid, Accelerated Phase / therapy. Male. Protein Kinase Inhibitors / pharmacology. Remission Induction. Transplantation, Homologous

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  • (PMID = 20657522.001).
  • [ISSN] 2329-0358
  • [Journal-full-title] Annals of transplantation
  • [ISO-abbreviation] Ann. Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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56. 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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  • [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.



57. 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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  • [Cites] J Biol Chem. 2000 May 19;275(20):15099-105 [10747872.001]
  • [Cites] Oncogene. 1992 Nov;7(11):2243-8 [1359494.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1031-7 [11287972.001]
  • [Cites] Science. 2001 Aug 3;293(5531):876-80 [11423618.001]
  • [Cites] J Biol Chem. 2001 Oct 26;276(43):39892-7 [11518717.001]
  • [Cites] Blood. 2002 May 1;99(9):3472-5 [11964322.001]
  • [Cites] Cancer Cell. 2002 May;1(4):339-53 [12086849.001]
  • [Cites] Cancer Cell. 2002 Aug;2(2):117-25 [12204532.001]
  • [Cites] Blood. 2002 Oct 15;100(8):3041-4 [12351420.001]
  • [Cites] Gastroenterology. 2002 Oct;123(4):1191-204 [12360481.001]
  • [Cites] Nat Rev Drug Discov. 2002 Oct;1(10):769-83 [12360255.001]
  • [Cites] Immunology. 2002 Dec;107(4):461-71 [12460191.001]
  • [Cites] Cancer Gene Ther. 2003 Jan;10(1):57-63 [12489029.001]
  • [Cites] Haematologica. 2003 Nov;88(11):1213-20 [14607749.001]
  • [Cites] Cancer Res. 2003 Nov 15;63(22):7834-9 [14633710.001]
  • [Cites] Oncogene. 2004 Jul 1;23(30):5161-74 [15122317.001]
  • [Cites] Oncogene. 2004 Oct 14;23(47):7854-62 [15334055.001]
  • [Cites] Br J Cancer. 2004 Nov 1;91(9):1735-41 [15494718.001]
  • [Cites] Nature. 1973 Jun 1;243(5405):290-3 [4126434.001]
  • [Cites] Science. 1986 Jul 11;233(4760):212-4 [3460176.001]
  • [Cites] EMBO J. 1986 Oct;5(10):2503-12 [2877871.001]
  • [Cites] Mol Cell Biol. 1991 Apr;11(4):1785-92 [2005881.001]
  • [Cites] Blood. 1991 Aug 15;78(4):921-9 [1651135.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Dec 1;90(23):11217-21 [8248231.001]
  • [Cites] Cancer Res. 1995 Jan 15;55(2):303-6 [7812962.001]
  • [Cites] Nat Med. 1996 May;2(5):561-6 [8616716.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jul 9;93(14):7263-8 [8692980.001]
  • [Cites] Oncogene. 1996 Jul 18;13(2):247-54 [8710363.001]
  • [Cites] EMBO J. 1997 Oct 15;16(20):6151-61 [9321394.001]
  • [Cites] Cancer Res. 1998 Aug 1;58(15):3353-61 [9699666.001]
  • [Cites] J Biol Chem. 1998 Sep 4;273(36):22877-83 [9722506.001]
  • [Cites] N Engl J Med. 1999 Jul 15;341(3):164-72 [10403855.001]
  • [Cites] Blood. 1999 Aug 1;94(3):1108-12 [10419904.001]
  • [Cites] Cell Prolif. 1994 Feb;27(2):63-71 [10465027.001]
  • [Cites] Cancer. 2005 Apr 15;103(8):1659-69 [15747376.001]
  • [Cites] Drug Discov Today. 2005 Aug 1;10(15):1041-7 [16055020.001]
  • [Cites] Leukemia. 2005 Oct;19(10):1774-82 [16136169.001]
  • [Cites] Blood. 2006 Jan 15;107(2):655-60 [16046527.001]
  • [Cites] Blood. 2006 Jan 15;107(2):669-78 [16166596.001]
  • [Cites] Mol Cell Biol. 2006 Mar;26(5):1754-69 [16478996.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1254-60 [16642049.001]
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6570-8 [16818629.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2407-15 [16763206.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 7;103(45):16870-5 [17077147.001]
  • [Cites] Endocr Rev. 2007 Feb;28(1):20-47 [16931767.001]
  • [Cites] Blood. 2007 Mar 1;109(5):2147-55 [17090651.001]
  • [Cites] J Pathol. 2007 Aug;212(4):402-10 [17503411.001]
  • [Cites] Clin Cancer Res. 2007 Oct 1;13(19):5834-40 [17908976.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2904-8 [18180382.001]
  • [Cites] Semin Oncol. 2008 Feb;35(1 Suppl 1):S1-17; quiz S18-20 [18346528.001]
  • [Cites] Oncogene. 2008 Jun 19;27(27):3831-44 [18246120.001]
  • [Cites] Science. 2000 Sep 15;289(5486):1938-42 [10988075.001]
  • (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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58. 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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59. Kantarjian H, Shah NP, Hochhaus A, Cortes J, Shah S, Ayala M, Moiraghi B, Shen Z, Mayer J, Pasquini R, Nakamae H, Huguet F, Boqué C, Chuah C, Bleickardt E, Bradley-Garelik MB, Zhu C, Szatrowski T, Shapiro D, Baccarani M: Dasatinib versus imatinib in newly diagnosed chronic-phase chronic myeloid leukemia. N Engl J Med; 2010 Jun 17;362(24):2260-70
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  • [Title] Dasatinib versus imatinib in newly diagnosed chronic-phase chronic myeloid leukemia.
  • BACKGROUND: Treatment with dasatinib, a highly potent BCR-ABL kinase inhibitor, has resulted in high rates of complete cytogenetic response and progression-free survival among patients with chronic myeloid leukemia (CML) in the chronic phase, after failure of imatinib treatment.
  • We assessed the efficacy and safety of dasatinib, as compared with imatinib, for the first-line treatment of chronic-phase CML.
  • METHODS: In a multinational study, 519 patients with newly diagnosed chronic-phase CML were randomly assigned to receive dasatinib at a dose of 100 mg once daily (259 patients) or imatinib at a dose of 400 mg once daily (260 patients).
  • The rate of major molecular response was higher with dasatinib than with imatinib (46% vs. 28%, P<0.0001), and responses were achieved in a shorter time with dasatinib (P<0.0001).
  • Progression to the accelerated or blastic phase of CML occurred in 5 patients who were receiving dasatinib (1.9%) and in 9 patients who were receiving imatinib (3.5%).
  • Since achieving complete cytogenetic response within 12 months has been associated with better long-term, progression-free survival, dasatinib may improve the long-term outcomes among patients with newly diagnosed chronic-phase CML. (ClinicalTrials.gov number, NCT00481247. )
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Chronic-Phase / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Benzamides. Blast Crisis / prevention & control. Dasatinib. Disease Progression. Female. Fusion Proteins, bcr-abl / antagonists & inhibitors. Humans. Imatinib Mesylate. Kaplan-Meier Estimate. Male. Middle Aged. Young Adult

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  • [Copyright] 2010 Massachusetts Medical Society
  • [CommentIn] Expert Opin Pharmacother. 2011 Jan;12(1):157-63 [21108601.001]
  • [CommentIn] N Engl J Med. 2010 Jun 17;362(24):2314-5 [20525994.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1672; author reply 1673-5 [20961253.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1673; author reply 1673-5 [20973146.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1673; author reply 1673-5 [20973145.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1672-3; author reply 1673-5 [20973144.001]
  • (PMID = 20525995.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00481247
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
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60. Notari M, Neviani P, Santhanam R, Blaser BW, Chang JS, Galietta A, Willis AE, Roy DC, Caligiuri MA, Marcucci G, Perrotti D: A MAPK/HNRPK pathway controls BCR/ABL oncogenic potential by regulating MYC mRNA translation. Blood; 2006 Mar 15;107(6):2507-16
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  • [Title] A MAPK/HNRPK pathway controls BCR/ABL oncogenic potential by regulating MYC mRNA translation.
  • Altered mRNA translation is one of the effects exerted by the BCR/ABL oncoprotein in the blast crisis phase of chronic myelogenous leukemia (CML).
  • Here, we report that in BCR/ABL+ cell lines and in patient-derived CML blast crisis mononuclear and CD34+ cells, p210(BCR/ABL) increases expression and activity of the transcriptional-inducer and translational-regulator heterogeneous nuclear ribonucleoprotein K (hnRNP K or HNRPK) in a dose- and kinase-dependent manner through the activation of the MAPK(ERK1/2) pathway.
  • Furthermore, HNRPK down-regulation and interference with HNRPK translation-but not transcription-regulatory activity impairs cytokine-independent proliferation, clonogenic potential, and in vivo leukemogenic activity of BCR/ABL-expressing myeloid 32Dcl3 and/or primary CD34+ CML-BC patient cells.
  • Mechanistically, we demonstrate that decreased internal ribosome entry site (IRES)-dependent Myc mRNA translation accounts for the phenotypic changes induced by inhibition of the BCR/ABL-ERK-dependent HNRPK translation-regulatory function.
  • Accordingly, MYC protein but not mRNA levels are increased in the CD34+ fraction of patients with CML in accelerated and blastic phase but not in chronic phase CML patients and in the CD34+ fraction of marrow cells from healthy donors.
  • Thus, BCR/ABL-dependent enhancement of HNRPK translation-regulation is important for BCR/ABL leukemogenesis and, perhaps, it might contribute to blast crisis transformation.

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  • [Cites] Exp Hematol. 1993 Oct;21(11):1460-6 [8405226.001]
  • [Cites] Mol Cell Biol. 2002 Apr;22(7):2255-66 [11884611.001]
  • [Cites] Med Oncol Tumor Pharmacother. 1992;9(3):139-47 [1341325.001]
  • [Cites] Nature. 1994 Apr 28;368(6474):867-71 [7512694.001]
  • [Cites] Mol Cell Biol. 1995 Mar;15(3):1324-32 [7862126.001]
  • [Cites] Cancer Res. 1995 Jun 1;55(11):2275-8 [7757976.001]
  • [Cites] Blood. 1995 Sep 15;86(6):2371-8 [7662984.001]
  • [Cites] Mol Cell Biol. 1995 Oct;15(10):5531-41 [7565705.001]
  • [Cites] Mol Cell Biol. 1996 May;16(5):2350-60 [8628302.001]
  • [Cites] J Biol Chem. 1996 Feb 16;271(7):3420-7 [8631943.001]
  • [Cites] Leukemia. 1996 May;10(5):751-6 [8656667.001]
  • [Cites] Leuk Res. 1996 Jan;20(1):85-91 [8632682.001]
  • [Cites] Blood. 1996 Aug 1;88(3):1005-12 [8704208.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 12;93(23):13137-42 [8917557.001]
  • [Cites] EMBO J. 1997 Jun 16;16(12):3587-98 [9218800.001]
  • [Cites] J Exp Med. 2001 Aug 6;194(3):275-84 [11489947.001]
  • [Cites] EMBO J. 2001 Dec 3;20(23):6793-804 [11726515.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):48-58 [11753385.001]
  • [Cites] Oncogene. 2001 Dec 13;20(57):8249-57 [11781839.001]
  • [Cites] Oncogene. 1997 Nov 6;15(19):2333-42 [9393877.001]
  • [Cites] Blood. 1998 Jan 15;91(2):406-18 [9427693.001]
  • [Cites] EMBO J. 1998 Aug 3;17(15):4442-55 [9687511.001]
  • [Cites] Oncogene. 1998 Sep 24;17(12):1597-606 [9794237.001]
  • [Cites] J Biol Chem. 1999 Mar 5;274(10):6553-8 [10037749.001]
  • [Cites] N Engl J Med. 1999 Apr 29;340(17):1330-40 [10219069.001]
  • [Cites] J Biol Chem. 1999 May 21;274(21):15101-9 [10329716.001]
  • [Cites] Proteomics. 2005 Feb;5(3):796-804 [15682461.001]
  • [Cites] Cell Death Differ. 2005 Jun;12(6):534-40 [15846378.001]
  • [Cites] Oncogene. 2005 Sep 22;24(42):6432-40 [16007188.001]
  • [Cites] Cancer Cell. 2005 Nov;8(5):355-68 [16286244.001]
  • [Cites] Ann Hematol. 2000 Aug;79(8):424-31 [10985361.001]
  • [Cites] Nat Cell Biol. 2001 Mar;3(3):325-30 [11231586.001]
  • [Cites] J Biol Chem. 2001 Mar 30;276(13):9699-704 [11121407.001]
  • [Cites] RNA. 2002 Mar;8(3):265-78 [12003487.001]
  • [Cites] Mol Cell Biol. 2002 Jul;22(13):4535-43 [12052863.001]
  • [Cites] Methods. 2002 Feb;26(2):191-8 [12054896.001]
  • [Cites] Oncogene. 2002 Oct 17;21(47):7137-46 [12370803.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):145-60 [12620409.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Aug;37(4):346-58 [12800146.001]
  • [Cites] Oncogene. 2003 Sep 11;22(39):8012-20 [12970749.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5716-22 [14522890.001]
  • [Cites] Curr Top Microbiol Immunol. 2004;279:169-97 [14560958.001]
  • [Cites] Oncogene. 2004 Mar 4;23(9):1693-703 [14647428.001]
  • [Cites] Annu Rev Immunol. 2004;22:247-306 [15032571.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3167-74 [15070699.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4010-22 [14982876.001]
  • [Cites] Cancer Treat Res. 2004;119:239-70 [15164881.001]
  • [Cites] Bioessays. 2004 Jun;26(6):629-38 [15170860.001]
  • [Cites] N Engl J Med. 2004 Aug 12;351(7):657-67 [15306667.001]
  • [Cites] Blood. 2004 Sep 1;104(5):1314-23 [15142884.001]
  • [Cites] Cancer Genet Cytogenet. 1987 Aug;27(2):349-56 [3474057.001]
  • [Cites] Leuk Res. 1988;12(6):507-16 [3165487.001]
  • [Cites] Cancer. 1988 Sep 15;62(6):1171-8 [3044574.001]
  • [Cites] Cell. 1992 Sep 18;70(6):901-10 [1525828.001]
  • [Cites] Leuk Lymphoma. 1993;11 Suppl 1:45-6 [8251915.001]
  • (PMID = 16293596.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / CA095512; United States / NCI NIH HHS / CA / CA16058
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; 0 / Ribonucleoproteins; 146410-60-8 / HNRNPK protein, human; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC1895740
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61. 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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  • [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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62. Etienne G, Milpied B, Réa D, Rigal-Huguet F, Tulliez M, Nicolini FE, French Intergroup of CML (Fi-LMC group): [Guidelines for the management of nilotinib (Tasigna)-induced side effects in chronic myelogenous leukemia: recommendations of French Intergroup of CML (Fi-LMC group)]. Bull Cancer; 2010 Aug;97(8):997-1009
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  • [Title] [Guidelines for the management of nilotinib (Tasigna)-induced side effects in chronic myelogenous leukemia: recommendations of French Intergroup of CML (Fi-LMC group)].
  • [Transliterated title] Recommandations du groupe Fi-LMC pour la gestion des effets indésirables du traitement par nilotinib (Tasigna) au cours de la leucémie myéloïde chronique.
  • Nilotinib (Tasigna) is a second-generation BCR-ABL kinase inhibitor, recently introduced and used for the treatment of chronic or accelerated phase CML patients, intolerant or resistant to imatinib.
  • This treatment represents and important step forward for the disease control of such patients but can lead to side effects, sometimes serious, which can limit its optimal use.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / adverse effects. Pyrimidines / adverse effects

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  • (PMID = 20529767.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Practice Guideline
  • [Publication-country] France
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Recombinant Proteins; 11096-26-7 / Erythropoietin; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
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63. Kim DH, Popradi G, Sriharsha L, Kamel-Reid S, Chang H, Messner HA, Lipton JH: No significance of derivative chromosome 9 deletion on the clearance kinetics of BCR/ABL fusion transcripts, cytogenetic or molecular response, loss of response, or treatment failure to imatinib mesylate therapy for chronic myeloid leukemia. Cancer; 2008 Aug 15;113(4):772-81
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  • [Title] No significance of derivative chromosome 9 deletion on the clearance kinetics of BCR/ABL fusion transcripts, cytogenetic or molecular response, loss of response, or treatment failure to imatinib mesylate therapy for chronic myeloid leukemia.
  • BACKGROUND: Although deletion of the derivative chromosome 9 (der 9; del-der 9) carries a poor prognosis in patients with chronic myeloid leukemia (CML) who are treated with hydroxyurea or interferon, its significance in patients on imatinib mesylate (IM) therapy is debated.
  • METHODS: In the current study, the authors used a locus-specific indicator breakpoint cluster region/receptor tyrosine kinase (BCR/ABL) probe to evaluate the significance of del-der 9 in 163 patients with CML who had fluorescence in situ hybridization (FISH) results available.
  • Serial changes in BCR/ABL fusion transcript levels also were monitored by using messenger RNA (mRNA) quantitative polymerase chain reaction (PCR).
  • The results of serial BCR/ABL mRNA quantitative PCR revealed similar patterns of BCR/ABL fusion gene reduction between the 2 groups.
  • CONCLUSIONS: The presence of del-der 9 in patients with CML did not influence 1) the response to IM therapy in terms of hematologic response, CyR, or MoR;. 2) LOR;.
  • 4) progression to accelerated phase/blast crisis; or 5) time to dose escalation of IM.
  • Therefore, the authors concluded that the detection of del-der 9 does not have an impact on the current management of patients with CML who are receiving IM therapy.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 9. Fusion Proteins, bcr-abl / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use



64. 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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  • [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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65. Kosugi N, Ebihara Y, Nakahata T, Saisho H, Asano S, Tojo A: CD34+CD7+ leukemic progenitor cells may be involved in maintenance and clonal evolution of chronic myeloid leukemia. Clin Cancer Res; 2005 Jan 15;11(2 Pt 1):505-11
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  • [Title] CD34+CD7+ leukemic progenitor cells may be involved in maintenance and clonal evolution of chronic myeloid leukemia.
  • PURPOSE: We analyzed CD34+ cells coexpressing CD7 in chronic myeloid leukemia (CML) in chronic phase (CP) or accelerated phase (AP) to clarify their role in progression or regression of the disease during treatment.
  • EXPERIMENTAL DESIGN: Enumeration of CD34+CD7+ cells was done on bone marrow nucleated cells from normal donors and CML patients.
  • Fluorescence in situ hybridization analysis was done on sorted CD34+CD7+and CD34+CD7- cells to examine the occupancy rate of each fraction by BCR-ABL+ cells with or without additional cytogenetic abnormalities.
  • RESULTS: The proportion of CD34+CD7+cells was significantly affected by the treatment outcome and/or the disease status as follows: 20.5 +/- 10.4% in normal donors (n = 22), 18.1 +/- 10.2% in CP with major cytogenetic response (n = 14), 53.0 +/- 12.9% in CP at diagnosis (n = 18), 55.0 +/- 15.8% in CP with minor or no cytogenetic response (n = 28), and 70.2 +/- 18.1% in AP (n = 6).
  • In six untreated CP patients, the ratio of BCR-ABL+ cells was comparable between each fraction.
  • In three patients with major cytogenetic response, the ratio of BCR-ABL+ cells was remarkably lower in CD34+CD7- cells than in CD34+CD7+cells.
  • CONCLUSIONS: Our results suggest that CD34+CD7+ cells may be involved in maintenance and clonal evolution of BCR-ABL+ cells in CML.
  • [MeSH-major] Antigens, CD34 / metabolism. Antigens, CD7 / metabolism. Hematopoietic Stem Cells / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Stem Cells / metabolism
  • [MeSH-minor] Adolescent. Adult. Bone Marrow. Chromosome Aberrations. Clone Cells. Cytogenetic Analysis. Disease Progression. Female. Fusion Proteins, bcr-abl / metabolism. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Tissue Donors



66. Huang Q: Chronic myelogenous leukemia in accelerated phase. Arch Pathol Lab Med; 2005 May;129(5):710
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  • [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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67. Yamamoto M, Kakihana K, Ohashi K, Yamaguchi T, Tadokoro K, Akiyama H, Sakamaki H: Serial monitoring of T315I BCR-ABL mutation by Invader assay combined with RT-PCR. Int J Hematol; 2009 May;89(4):482-8
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  • [Title] Serial monitoring of T315I BCR-ABL mutation by Invader assay combined with RT-PCR.
  • We recently developed an Invader assay combined with reverse transcriptase polymerase-chain-reaction in order to quantify T315I bcr-abl transcripts.
  • Using this assay, we serially monitored T315I bcr-abl transcripts in chronic myeloid leukemia (CML) patients whose bcr-abl transcripts were still detectable at 6 months after starting imatinib therapy.
  • Although, we continued to monitor bcr-abl transcripts in 14 CML patients (13 chronic phases and 1 accelerated phase) for up to 12 months, there were no patients who were apparently resistant to imatinib due to the T315I mutation.
  • In contrast, in a case of Philadelphia chromosome-positive acute lymphoid leukemia being treated with chemotherapy including imatinib, we monitored both wild-type and T315I bcr-abl transcripts, and found increased levels of T315I transcripts during relapse (0% at the time of diagnosis and 54.8% at relapse).
  • [MeSH-major] Fusion Proteins, bcr-abl / analysis. Fusion Proteins, bcr-abl / genetics. Genetic Techniques
  • [MeSH-minor] Adult. Aged. Female. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Male. Middle Aged. Mutation / genetics

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  • [Cites] Blood. 2006 Jul 1;108(1):28-37 [16522812.001]
  • [Cites] Clin Cancer Res. 2006 Dec 15;12(24):7374-9 [17189410.001]
  • [Cites] Blood. 2005 Sep 15;106(6):2128-37 [15914554.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1321-31 [15215876.001]
  • [Cites] Mol Diagn. 1999 Dec;4(4):353-64 [10671646.001]
  • [Cites] Leukemia. 2002 Nov;16(11):2190-6 [12399961.001]
  • [Cites] Blood. 2007 Dec 1;110(12):4005-11 [17785585.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):1007-14 [16424036.001]
  • [Cites] Science. 2004 Jul 16;305(5682):399-401 [15256671.001]
  • [Cites] Hematology. 2001;6(4):261-5 [27414845.001]
  • [Cites] Blood. 2007 Jan 15;109(2):500-2 [16990603.001]
  • [Cites] Leuk Res. 2005 Sep;29(9):1073-7 [16038734.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jul 18;97(15):8272-7 [10890904.001]
  • [Cites] Haematologica. 2008 Feb;93(2):186-92 [18223278.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1328-33 [16614241.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2332-8 [16772610.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2926-32 [15256429.001]
  • [Cites] Blood. 2008 Jul 1;112(1):53-5 [18403620.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4611-4 [12576318.001]
  • [Cites] Clin Biochem. 2004 Apr;37(4):268-76 [15003728.001]
  • [Cites] N Engl J Med. 2003 May 29;348(22):2265-6 [12773665.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 1;102(9):3395-400 [15705718.001]
  • [Cites] Curr Opin Genet Dev. 2006 Feb;16(1):92-9 [16343892.001]
  • (PMID = 19343480.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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68. Latagliata R, Breccia M, Carmosino I, Sarlo C, Montefusco E, Mancini M, Natalino F, Chistolini A, De Cuia R, Russo E, Morano GS, Biondo F, Spadea A, Mandelli F, Alimena G: Elderly patients with Ph+ chronic myelogenous leukemia (CML): results of imatinib mesylate treatment. Leuk Res; 2005 Mar;29(3):287-91
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  • [Title] Elderly patients with Ph+ chronic myelogenous leukemia (CML): results of imatinib mesylate treatment.
  • Thirty-five patients with Ph+ CML aged more than 60 years were treated with imatinib.
  • Twenty-four patients (group A) were in late chronic phase (CP) and eleven patients (group B) were in accelerated/blastic phase (AP/BP).
  • In group A, complete haematological response (CHR) was achieved by all patients; seventeen patients (70.8%) attained a complete cytogenetic response (CCR), one (4.1%) attained a partial CR, one (4.1%) a minor CR (Ph+ 70%) and five (21%) were resistant (Ph+ 100%), toxicity was mild: seven patients had a transient cytopenia, three a skin reaction, one a moderate oedema and one muscular pain.
  • In group B, one patient died after 3 months in aplastic phase from sepsis, three patients were resistant and seven patients (63.7%) achieved CHR; of these, four obtained CCR.
  • After a median follow-up of 17 months, 4 patients have died from progressive disease, 6 are alive; 1 in AP and 5 in CHR (4 of them being in CCR).
  • [MeSH-major] Aged. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use

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  • [ErratumIn] Leuk Res. 2005 Sep;29(9):1099. Roberto, Latagliata [corrected to Latagliata, Roberto]; Massimo, Breccia [corrected to Breccia, Massimo]; Ida, Carmosino [corrected to Carmosino, Ida]; Chiara, Sarlo [corrected to Sarlo, Chiara]; Enrico, Montefusco [corrected to Montefusco, Enrico]; Marco, Mancini [corrected to Mancini, Marco]; Fiammetta, Natalino [corrected to Natalino, Fiammetta]; Antonio, Chistolini [corrected to Chistolini, Antonio]; Rosa, De Cuia [corrected to De Cuia, Rosa]; Eleonora, Russo [corrected to Russo, Eleonora]; Giacomo, Morano Salvatore [corrected to Morano, Giacomo Salvatore]; Francesca, Biondo [corrected to Biondo, Francesca]; Antonio, Spadea [corrected to Spadea, Antonio]; Franco, Mandelli [corrected to Mandelli, Franco]; Giuliana, Alimena [corrected to Alimena, Giuliana]
  • (PMID = 15661264.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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69. 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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  • [Cites] J Clin Oncol. 2009 Dec 10;27(35):6041-51 [19884523.001]
  • [Cites] Leukemia. 2008 Oct;22(10):1963-6 [18754023.001]
  • [Cites] J Exp Med. 2007 Mar 19;204(3):461-5 [17353369.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1031-7 [11287972.001]
  • [Cites] Science. 1986 Jul 11;233(4760):212-4 [3460176.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1200-6 [18401416.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1038-42 [11287973.001]
  • [Cites] Baillieres Clin Haematol. 1987 Dec;1(4):907-29 [3332856.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3540-6 [17715389.001]
  • [Cites] J Assoc Physicians India. 2007 Feb;55:103-7 [17571738.001]
  • [Cites] Nature. 1973 Jun 1;243(5405):290-3 [4126434.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1809-20 [16709930.001]
  • [Cites] Wien Klin Wochenschr. 2008;120(21-22):697-709 [19116712.001]
  • [Cites] N Engl J Med. 2006 Dec 7;355(23):2408-17 [17151364.001]
  • [Cites] J Clin Oncol. 2008 Jul 10;26(20):3358-63 [18519952.001]
  • [Cites] N Engl J Med. 2003 Mar 13;348(11):994-1004 [12637609.001]
  • [Cites] Leukemia. 2009 Jun;23(6):1054-61 [19282833.001]
  • [Cites] Nat Med. 1996 May;2(5):561-6 [8616716.001]
  • (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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70. 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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71. 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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  • [Cites] Blood. 2003 Jul 1;102(1):31-5 [12595317.001]
  • [Cites] Br J Haematol. 1998 Sep;102(5):1376-9 [9753074.001]
  • [Cites] N Engl J Med. 2003 Oct 9;349(15):1423-32 [14534335.001]
  • [Cites] Science. 2004 Mar 5;303(5663):1483-7 [15001769.001]
  • [Cites] Br J Cancer. 2004 Mar 22;90(6):1265-73 [15026811.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4010-22 [14982876.001]
  • [Cites] Br J Haematol. 2004 Jun;125(6):729-42 [15180862.001]
  • [Cites] N Engl J Med. 2004 Aug 12;351(7):657-67 [15306667.001]
  • [Cites] Blood. 2004 Oct 1;104(7):2204-5 [15377577.001]
  • [Cites] Cell. 2004 Oct 29;119(3):431-43 [15507213.001]
  • [Cites] Blood. 1999 Dec 15;94(12):4370-3 [10590083.001]
  • [Cites] FEBS Lett. 2000 Jan 28;466(2-3):367-71 [10682862.001]
  • [Cites] Blood. 2000 Mar 1;95(5):1758-66 [10688835.001]
  • [Cites] Blood. 2000 Mar 15;95(6):2126-31 [10706884.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3498-505 [10828035.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1031-7 [11287972.001]
  • [Cites] Nat Biotechnol. 2001 Apr;19(4):342-7 [11283592.001]
  • [Cites] Br J Haematol. 2001 Mar;112(4):916-26 [11298586.001]
  • [Cites] Genes Dev. 2001 Jul 1;15(13):1625-30 [11445537.001]
  • [Cites] Oncogene. 2001 Dec 13;20(57):8249-57 [11781839.001]
  • [Cites] Leukemia. 2002 Aug;16(8):1402-11 [12145676.001]
  • [Cites] Mol Cell Biol. 2002 Sep;22(18):6393-405 [12192039.001]
  • [Cites] Cancer Cell. 2002 Aug;2(2):117-25 [12204532.001]
  • [Cites] J Biol Chem. 2002 Oct 18;277(42):39209-16 [12161443.001]
  • [Cites] Oncogene. 2002 Dec 9;21(56):8629-42 [12476309.001]
  • [Cites] Oncogene. 2003 Jun 19;22(25):3952-63 [12813469.001]
  • [Cites] Blood. 1984 Apr;63(4):789-99 [6584184.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Aug;87(15):5802-6 [2198571.001]
  • [Cites] J Biol Chem. 1991 Aug 5;266(22):14183-7 [1860835.001]
  • [Cites] Oncogene. 1991 Oct;6(10):1899-902 [1923513.001]
  • [Cites] Development. 1993 Oct;119(2):433-46 [7904558.001]
  • [Cites] Blood. 1994 Jun 15;83(12):3449-56 [8204873.001]
  • [Cites] Mol Cell Biol. 1994 Sep;14(9):5692-700 [8065305.001]
  • [Cites] Mol Cell Biol. 1995 Nov;15(11):6075-87 [7565760.001]
  • [Cites] Cell. 1996 Sep 6;86(5):731-41 [8797820.001]
  • [Cites] Leukemia. 1997 Jan;11(1):151-2 [9001431.001]
  • [Cites] Br J Haematol. 1997 Oct;99(1):30-5 [9359498.001]
  • [Cites] Neuron. 1998 Dec;21(6):1259-72 [9883720.001]
  • [Cites] N Engl J Med. 1999 Jul 15;341(3):164-72 [10403855.001]
  • [Cites] Ann Intern Med. 1999 Aug 3;131(3):207-19 [10428738.001]
  • [Cites] J Clin Oncol. 1999 Jan;17(1):284-92 [10458244.001]
  • [Cites] Exp Cell Res. 2005 Jan 1;302(1):129-42 [15541732.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4100-9 [15867198.001]
  • [Cites] Cell. 2005 Sep 23;122(6):835-47 [16179254.001]
  • [Cites] Blood. 2006 Jan 1;107(1):205-12 [16144796.001]
  • [Cites] Blood. 2001 Apr 15;97(8):2440-8 [11290609.001]
  • [Cites] Blood. 2003 Jul 1;102(1):276-83 [12623848.001]
  • (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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72. De Souza CA, Vigorito AC, Ruiz MA, Nucci M, Dulley FL, Funcke V, Tabak D, Azevedo AM, Byington R, Macedo MC, Saboya R, Penteado Aranha FJ, Oliveira GB, Zulli R, Martins Miranda EC, Azevedo WM, Lodi FM, Voltarelli JC, Simões BP, Colturato V, De Souza MP, Silla L, Bittencourt H, Piron-Ruiz L, Maiolino A, Gratwohl A, Pasquini R: Validation of the EBMT risk score in chronic myeloid leukemia in Brazil and allogeneic transplant outcome. Haematologica; 2005 Feb;90(2):232-7
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  • [Title] Validation of the EBMT risk score in chronic myeloid leukemia in Brazil and allogeneic transplant outcome.
  • BACKGROUND AND OBJECTIVES: The management of chronic myeloid leukemia (CML) has changed radically since the introduction of imatinib therapy.
  • The aim of this retrospective analysis of 1,084 CML patients who received an allogeneic HSCT in 10 Brazilian Centers between February 1983 and March 2003 was to validate the EBMT risk score.
  • DESIGN AND METHODS: The study population comprised 647 (60%) males and 437 (40%) females, with a median age of 32 years old (range 1 - 59); 898 (83%) were in chronic phase, 146 (13%) were in accelerated phase and 40 (4%) were in blast crisis; 151 (14%) were younger than 20 years old, 620 (57%) were between 20 and 40 and 313 (29%) were older than 40; 1,025 (94%) received an HLA fully matched sibling transplant and only 59 (6%) received an unrelated transplant.
  • The interval from diagnosis to transplantation was less than 12 months in 223 (21%) cases and greater in 861 (79%).
  • The overall survival, disease-free survival, transplant-related mortality and relapse incidence were 49%, 50%, 45% and 25%, respectively.
  • Disease-free survival (DFS) and transplant related mortality (TRM) in a patients with a score of 3 or more were 46% and 49%, respectively and the relapse rate beyond score 5-6 was 77%.
  • Disease status had a negative impact on all outcomes (OS, DFS, TRM, and relapse).
  • DFS and TRM were significant for disease phase and female donor-male recipient (p<0.001 and p<0.003, respectively).
  • In our experience, age and interval between diagnosis and transplant did influence OS, DFS, TRM, and relapse rate.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy
  • [MeSH-minor] Adolescent. Adult. Brazil. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Middle Aged. Retrospective Studies. Risk. Sex Factors. Transplantation, Homologous. Treatment Outcome



73. Mai YJ, Qiu LG, Li ZJ, Yu Z, Li CH, Wang YF, Wang GR, Li Q: [The expression of beta-catenin and its significance in leukemia cells]. Zhonghua Xue Ye Xue Za Zhi; 2007 Aug;28(8):541-4
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  • [Title] [The expression of beta-catenin and its significance in leukemia cells].
  • OBJECTIVE: To investigate the expression of beta-catenin in patients with leukemia and explore its significance in leukemias.
  • METHODS: RT-PCR was used to detect the expression of beta-catenin in bone marrow mononuclear cells (BMMNCs) from patients with leukemia.
  • RESULTS: Expression of beta-catenin was statistically higher in acute myeloid leukemia (AML) and acute lymphocytic leukemia (ALL) samples than in normal donors (P = 0.001 and 0.016 respectively) and chronic phase chronic myeloid leukemia (CML) patients (P = 0.001 and P = 0.008 respectively), while there was no statistic difference between AML and ALL patients (P = 0.58).
  • In addition, beta-catenin expression in chronic phase CML patients was like that in normal donors (P = 0.49), but increased significantly in blast crisis and accelerated phase.
  • Immunocytochemical analysis revealed that BMMNCs from normal donors expressed beta-catenin on the plasma membrane and cytoplasma, while those from acute leukemia expressed beta-catenin to varying degrees in the nucleus as well.
  • No clinical features, such as, age, initial WBC count, therapy response rate, blast cell numbers or cytogenetic risk was found to be correlated with the expression of beta-catenin excepting for CD34+ positive rate (P = 0.004) in AML.
  • CONCLUSION: As a key mediator of Wnt signal transduction way, overexpression of beta-catenin in leukemia cells indicates that it might be aberrantly activated in acute leukemia, accelerated or blastic phase of CML.
  • [MeSH-major] Leukemia / metabolism. beta Catenin / metabolism

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  • (PMID = 18078131.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / beta Catenin
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74. Bornhäuser M, Kröger N, Schwerdtfeger R, Schafer-Eckart K, Sayer HG, Scheid C, Stelljes M, Kienast J, Mundhenk P, Fruehauf S, Kiehl MG, Wandt H, Theuser C, Ehninger G, Zander AR, Cooperative German Transplant Study Group: Allogeneic haematopoietic cell transplantation for chronic myelogenous leukaemia in the era of imatinib: a retrospective multicentre study. Eur J Haematol; 2006 Jan;76(1):9-17
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  • [Title] Allogeneic haematopoietic cell transplantation for chronic myelogenous leukaemia in the era of imatinib: a retrospective multicentre study.
  • OBJECTIVE: To analyse the results of allogeneic haematopoietic cell transplantation (HCT) in patients with advanced stages of Philadelphia chromosome-positive chronic myelogenous leukaemia (CML) who had previously been treated with imatinib mesylate (IM).
  • METHODS: We analysed the outcome of 61 patients with CML who had received allogeneic HCT from sibling (n = 18) or unrelated (n = 43) donors after having been treated with IM.
  • Forty-one patients had received IM because of accelerated or blast phase CML.
  • RESULTS: The incidence of grades II-IV and III-IV graft-versus-host disease was 66% and 38% respectively.
  • The probability of overall survival (OS), disease-free survival (DFS) and relapse at 18 months for the whole patient cohort were 37%, 33% and 24% respectively.
  • Univariate analysis showed that fludarabine-based conditioning therapy, age > or = 40 yr and >12 months interval between diagnosis and transplantation were associated with a significantly lower OS and DFS and a higher NRM.
  • CONCLUSION: These data suggest that although pretreatment with IM is not an independent negative prognostic factor, it cannot improve the dismal prognosis of CML patients at high risk for transplant-related mortality.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Transplantation Conditioning
  • [MeSH-minor] Adolescent. Adult. Benzamides. Busulfan / administration & dosage. Cohort Studies. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Disease-Free Survival. Female. Graft vs Host Disease / etiology. Graft vs Host Disease / mortality. Humans. Imatinib Mesylate. Male. Middle Aged. Myeloablative Agonists / administration & dosage. Recurrence. Retrospective Studies. Risk Factors. Transplantation, Homologous. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Whole-Body Irradiation

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  • (PMID = 16343266.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Myeloablative Agonists; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
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75. Li X, Yang J, Chen X, Liu J, Li H, Zheng J, He Y, Chen Z, Huang S: A report of early cytogenetic response to imatinib in two patients with chronic myeloid leukemia at accelerated phase and carrying the e19a2 BCR-ABL transcript. Cancer Genet Cytogenet; 2007 Jul 15;176(2):166-8
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  • [Title] A report of early cytogenetic response to imatinib in two patients with chronic myeloid leukemia at accelerated phase and carrying the e19a2 BCR-ABL transcript.
  • The development of imatinib is a milestone in the treatment of chronic myeloid leukemia (CML), and its therapeutic effect has been extensively investigated in CML patients carrying M-bcr and m-bcr BCR/ABL fusion transcripts.
  • However, our knowledge about its therapeutic effect on CML patients with rare BCR/ABL fusion transcripts e19a2(u-bcr) remains sparse.
  • Here, we report on two CML patients with e19a2 transcripts who rapidly progressed into the accelerated phase, further confirming the possibility that 19a2 might be associated with an unfavorable prognosis in CML.
  • [MeSH-major] Gene Expression Regulation, Leukemic / drug effects. Genes, abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Benzamides. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Cytogenetic Analysis. Disease Progression. Exons. Female. Humans. Imatinib Mesylate. Male. Middle Aged. RNA, Messenger / drug effects. RNA, Messenger / metabolism. Time Factors. Translocation, Genetic. Treatment Outcome

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  • (PMID = 17656262.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate
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76. Burchert A: Roots of imatinib resistance: a question of self-renewal? Drug Resist Updat; 2007 Aug-Oct;10(4-5):152-61
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  • The BCR-ABL-fusion gene is critical for the development of chronic myeloid leukemia (CML) and BCR-ABL positive acute lymphatic leukemia (Ph+ ALL).
  • Blocking BCR-ABL by the ABL tyrosine kinase inhibitor imatinib mesylate (IM, Gleevec) is clinically highly efficient.
  • Treatment response is unfortunately compromised by the emergence of IM resistance, which is regularly seen in accelerated and blastic phase of CML (CML-AP/BP) and in Ph+ ALL.
  • BCR-ABL kinase domain mutations are then considered the causative mechanism of IM resistance, because 50-60% of the IM resistant patients harbour such mutations.
  • In contrast, IM resistance arises very rarely in patients that are treated with IM in early chronic phase of CML.
  • This implies that BCR-ABL independent factors such as the cellular context of BCR-ABL expression and stage of disease decisively control the evolution of IM resistance.
  • In line with this, novel Abl-kinase inhibitors such as dasatinib (DA) or nilotinib (NI) - although capable of inhibiting most of the BCR/-BL kinase mutants - still often fail to overcome resistance and do mostly not induce durable cytogenetic responses in IM resistant CML-AP/BC and Ph+ ALL patients.
  • On the basis of available evidence it is proposed here that alternative genetic aberrations, which synergize with BCR-ABL to enable leukemic self-renewal are of causal importance for the evolution of clinical kinase inhibitor resistance.
  • [MeSH-major] Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Benzamides. Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Models, Biological. Mutation

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  • (PMID = 17683977.001).
  • [ISSN] 1368-7646
  • [Journal-full-title] Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy
  • [ISO-abbreviation] Drug Resist. Updat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 104
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77. Wang JX, Huang XJ, Wu DP, Hu JD, Liu T, Hu Y, Meng FY, Chen XQ, Hou M, Li Y, Wang SJ, Wang JM, Ren HY, Yu L, Chen FY, Qiu LG, Jiang B, Sun AN, Liu TB, Zhu HL, Guo T, Xu D, Ji CY, Lü XY, Jiao L, Song XM, Huang HH: [Overview of chronic myelogenous leukemia and its current diagnosis and treatment patterns in 15 hospitals in China.]. Zhonghua Xue Ye Xue Za Zhi; 2009 Nov;30(11):721-5
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  • [Title] [Overview of chronic myelogenous leukemia and its current diagnosis and treatment patterns in 15 hospitals in China.].
  • OBJECTIVE: To explore demographic characteristics, current diagnosis and treatment patterns of chronic myelogenous leukemia (CML) patients in China.
  • METHODS: Data of hospitalized CML patients in 2005 whole year and outpatient information (July 1 through September 30, 2006) from 15 hospitals throughout China were analyzed.
  • RESULTS: A total of 1824 CML cases were analyzed, including 722 inpatients and 1102 outpatients.
  • The median age at diagnosis was 40.02 (2.45 - 83.29) years old, 90.41% of the patients were diagnosed at chronic phase.
  • Proportion of accelerated phase or blast crisis patients increased to 21.66% during study period.
  • 93.20% of the patients received blood routine and bone marrow morphologic examination at diagnosis and in monitoring; 70.29% were performed cytogenetic analysis and 51.54% performed molecular measurement in addition.
  • The most common therapy for CML treatment was hydroxycarbamide.
  • The proportions of accelerated phase and blast crisis patients treated with imatinib were 48.28% and 48.42%, respectively, being significantly higher than that of chronic phase patients (35.9%) (P < 0.05).
  • CONCLUSIONS: CML in China tends to afflict younger population than in Western countries.
  • Most patients were diagnosed in the chronic phase.
  • Due to restriction of financial support, only one third of CML patients were treated with imatinib, and the majority of the treated were not monitored in time.
  • Clinicians should pay attention to resistance and intolerance to imatinib treatment in accelerated phase or blast crisis patients.
  • [MeSH-minor] Benzamides / therapeutic use. China. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy

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  • (PMID = 20137304.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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78. 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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79. Giles FJ, DeAngelo DJ, Baccarani M, Deininger M, Guilhot F, Hughes T, Mauro M, Radich J, Ottmann O, Cortes J: Optimizing outcomes for patients with advanced disease in chronic myelogenous leukemia. Semin Oncol; 2008 Feb;35(1 Suppl 1):S1-17; quiz S18-20
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  • [Title] Optimizing outcomes for patients with advanced disease in chronic myelogenous leukemia.
  • The treatment of chronic myelogenous leukemia (CML) has been revolutionized by the development of the small-molecule tyrosine kinase inhibitor imatinib.
  • The primary target for this drug is the oncogenic BCR-ABL kinase.
  • Five-year survival rates for patients in chronic phase CML is now greater than 80%.
  • Patients who have advanced beyond the chronic phase to the accelerated phase or blast crisis, however, have not faired as well.
  • Progression occurs for a variety of reasons, including late diagnosis, slow response to imatinib, and the development of imatinib-resistant clones.
  • Imatinib resistance has, in part, been addressed with the introduction of the new BCR-ABL inhibitors, namely dasatinib and nilotinib.
  • These drugs have shown efficacy in CML patients with wild-type BCR-ABL and some BCR-ABL mutants that are imatinib-resistant.
  • Unfortunately, some BCR-ABL mutations remain resistant to these therapies and will require the development of alternative treatments, and other mechanisms of imatinib resistance besides BCR-ABL mutation exist.
  • More aggressive therapies are being considered for high-risk patients, including increased dosage of the current tyrosine kinase inhibitors, along with combination therapies.
  • Aggressive therapy holds promise, as the data suggest that responses are improved.
  • This is especially important for young CML patients, who hopefully will remain in remission for decades.
  • Polymerase chain reaction analysis has become of primary importance as a means of assessing disease burden, and given the idiosyncrasies of this technique, standards must be established to allow results to be compared across different institutions.
  • Additionally, the nature of advanced disease is being explored.
  • Increased activity of these pathways correlates with poor response and eventual disease progression.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / therapeutic use

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  • (PMID = 18346528.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins c-jun; 0 / Wnt Proteins; 0 / beta Catenin
  • [Number-of-references] 131
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80. Nicolini FE, Corm S, Lê QH, Sorel N, Hayette S, Bories D, Leguay T, Roy L, Giraudier S, Tulliez M, Facon T, Mahon FX, Cayuela JM, Rousselot P, Michallet M, Preudhomme C, Guilhot F, Roche-Lestienne C: Mutation status and clinical outcome of 89 imatinib mesylate-resistant chronic myelogenous leukemia patients: a retrospective analysis from the French intergroup of CML (Fi(phi)-LMC GROUP). Leukemia; 2006 Jun;20(6):1061-6
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  • [Title] Mutation status and clinical outcome of 89 imatinib mesylate-resistant chronic myelogenous leukemia patients: a retrospective analysis from the French intergroup of CML (Fi(phi)-LMC GROUP).
  • The emergence of ABL point mutations is the most frequent cause for imatinib resistance in chronic myelogenous leukemia (CML) patients and can occur during any phase of the disease; however, their clinical impact remains controversial.
  • In this study, we retrospectively analyzed the predictive impact of 94 BCR-ABL kinase domain mutations (18 T315I, 26 P-loop, 50 in other sites) found in 89 imatinib-resistant CML patients.
  • At imatinib onset, 64% of patients (57/89) were in chronic phase (CP), 24% (21/89) in accelerated phase (AP) and 12% (11/89) in blastic phase (BP).
  • T315I and P-loop mutations were preferentially discovered in accelerated phase of BP CML, and other types of mutations in CP (P=0.003).
  • Therefore, P-loop and T315I mutations selectively impair the outcome of imatinib-resistant CML patients, in contrast to other mutations, which may benefit from dose escalation of imatinib, able to improve or stabilize disease response.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Point Mutation. Pyrimidines / therapeutic use



81. 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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82. 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



83. Walther JU, Pohl I, Rausch A, Fuehrer M: Proliferation studies on chromosome preparations of bone marrow in hematological disease. Oncol Rep; 2006 Oct;16(4):893-9
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  • [Title] Proliferation studies on chromosome preparations of bone marrow in hematological disease.
  • The disorders studied were: Acute lymphoblastic leukemia (ALL) (N=107), chronic myeloid leukemia (CML) (N=166) and aplastic anemia in childhood (AA) (N=39).
  • ii) CML: Philadelphia-positive CML shows proliferation activities quite distinct from Philadelphia-negative CML; however there is only a small change in the proliferative activity from the chronic phase to the accelerated phase or blast crisis.
  • Higher levels at diagnosis are associated with a faster and better response to therapy.
  • In conclusion, assessment of the proliferative activity in cytogenetic preparations made from bone marrow samples of patients with haematological disease may add valuable information as to diagnostic sub-groups and clinical course and may contribute to therapeutic decisions.
  • [MeSH-major] Bone Marrow Cells / cytology. Chromosomes / ultrastructure. Hematologic Neoplasms / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 16969511.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
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84. 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



85. Takagi Y, Aota Y, Gotoh A, Sakurai M: [Effect of low-dose dasatinib in an elderly patient with chronic myelogenous leukemia (CML)]. Gan To Kagaku Ryoho; 2010 Nov;37(11):2213-5
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  • [Title] [Effect of low-dose dasatinib in an elderly patient with chronic myelogenous leukemia (CML)].
  • We experienced a case of chronic myelogenous leukemia (CML) treated successfully with low-dose dasatinib (20 mg/day).
  • An 87-year-old man was diagnosed with CML in January 2003 and was given imatinib (200 mg/day).
  • However, since the blood count was poorly controlled with HU, treatment with dasatinib, one of the second-generation tyrosine kinase inhibitors, was started at the accelerated phase (AP) in June 2009.
  • Dasatinib was given in a daily dose of 20 mg, intending dose escalation after confirmation of its safety.
  • Low-dose dasatinib might be a useful treatment in the control of selected patients with CML.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Thiazoles / administration & dosage

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  • (PMID = 21084830.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
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86. Otero L, Ornellas MH, de Azevedo AM, Tavares Rde C, Pires V, Abdelhay E, Bouzas LF, Fernandez Tde S: Karyotype abnormalities and their clinical significance in a group of chronic myeloid leukemia patients treated with hematopoietic stem cell transplantation. Sao Paulo Med J; 2007 Jul 5;125(4):246-9
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  • [Title] Karyotype abnormalities and their clinical significance in a group of chronic myeloid leukemia patients treated with hematopoietic stem cell transplantation.
  • CONTEXT AND OBJECTIVE: Following hematopoietic stem cell transplantation (HSCT), karyotyping is a valuable tool for monitoring engraftment and disease status.
  • Few studies have examined the prognostic significance of karyotypes in patients who underwent HSCT for chronic myeloid leukemia (CML).
  • The objective of this study was to evaluate the significance of pretransplantation cytogenetic status in relation to outcomes following HSCT in CML patients.
  • DESIGN AND SETTING: Case series study at Instituto Nacional do Câncer (INCA), Rio de Janeiro, Brazil.
  • RESULTS: Thirty-one patients were in the chronic phase and eight were in the accelerated phase.
  • [MeSH-major] Chromosome Aberrations. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Philadelphia Chromosome



87. Forrest DL, Trainor S, Brinkman RR, Barnett MJ, Hogge DE, Nevill TJ, Shepherd JD, Nantel SH, Toze CL, Sutherland HJ, Song KW, Lavoie JC, Power MM, Abou-Mourad Y, Smith CA: Cytogenetic and molecular responses to standard-dose imatinib in chronic myeloid leukemia are correlated with Sokal risk scores and duration of therapy but not trough imatinib plasma levels. Leuk Res; 2009 Feb;33(2):271-5
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  • [Title] Cytogenetic and molecular responses to standard-dose imatinib in chronic myeloid leukemia are correlated with Sokal risk scores and duration of therapy but not trough imatinib plasma levels.
  • Cytogenetic and molecular responses to standard-dose imatinib (IM) were correlated with trough IM plasma levels for 78 patients with chronic myeloid leukemia (CML) after a minimum of 12 months of IM therapy.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / blood. Pyrimidines / blood
  • [MeSH-minor] Adult. 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



88. Wang AH, Wang YY, Yao Y, Xu ZZ, Zhou L, Wang L, Zhang L, Chen Y, Shen ZX, Hu J, Li JM: Summary of 615 patients of chronic myeloid leukemia in Shanghai from 2001 to 2006. J Exp Clin Cancer Res; 2010;29:20
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  • [Title] Summary of 615 patients of chronic myeloid leukemia in Shanghai from 2001 to 2006.
  • BACKGROUND: To retrospectively review the incidence, treatment efficacy, we followed up newly diagnosed chronic myelogenous leukemia (CML) patients residing in Shanghai during 2001-2006.
  • CML mainly afflicted those aged 40-60 years old and was slightly more frequent in males than females.
  • More than 85% of the patients were in chronic phase (CP) when diagnosed.
  • With the median follow-up of 18 months, imatinib treatment induced 92.2% complete hematologic responses, and 64.3% complete cytogenetic responses among CML-CP patients.
  • Meanwhile, in the imatinib group, all response rates of patients in CP were significantly greater than that in accelerated or blastic crisis phase.
  • As the first-line regime for CML, imatinib was less administered in Shanghai before, but has received considerable development and great responses since 2003.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Benzamides. China. Disease-Free Survival. Female. Humans. Imatinib Mesylate. Incidence. Male. Middle Aged. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Retrospective Studies. Treatment Outcome



89. Ghaith F, Abdou S, El-Bendary A, Shahin D, Eid M, Megeed WA, El-Sheikh I, Farrag W, Yousuf S: Prognostic relevance of 9q34 deletion and the suppressor of cytokine signalling-1 in CML patients. Int J Lab Hematol; 2010 Feb;32(1 Pt 2):103-12
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  • [Title] Prognostic relevance of 9q34 deletion and the suppressor of cytokine signalling-1 in CML patients.
  • Chronic myeloid leukemia (CML) is characterized by formation of the BCR/ABL fusion gene.
  • This study aims to determine the incidence and prognostic value of the 9q34 deletion using fluorescence in situ hybridization and SOCS-1 mRNA aberrant expression by PCR in 43 CML patients at different phases of the disease and in 10 normal controls and correlate the data to interferon response.
  • All patients were Philadelphia-positive, deletions of 9q34 were observed in 20.9% of all patients (13.3% chronic phase, 10% accelerated phase and 33.3% in blast crisis).
  • SOCS expressions were positive in 53.4% of all patients (40% chronic phase, 50% AP and 66.67% in blast crisis).
  • Deletion of 9q34 and aberrant expression of SOCS-1 are associated with poor prognosis in CML patients with different phases of the disease under interferon therapy.
  • [MeSH-major] Chromosome Deletion. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Suppressor of Cytokine Signaling Proteins / genetics
  • [MeSH-minor] Disease-Free Survival. Humans. In Situ Hybridization, Fluorescence. Polymerase Chain Reaction. Prognosis. RNA, Messenger / metabolism

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  • (PMID = 19222642.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Suppressor of Cytokine Signaling Proteins
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90. Vidović A, Janković G, Colović M, Tomin D, Perunicić M, Bila J, Marković O, Bosković D: The proto-oncogene expression varies over the course of chronic myeloid leukemia. Hematology; 2008 Feb;13(1):34-40
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  • [Title] The proto-oncogene expression varies over the course of chronic myeloid leukemia.
  • The chronic phase (CP) of chronic myeloid leukemia (CML) is characterized by the expression of chimeric BCR/ABL gene, extended survival, and profligate growth of maturing granulocyte stemline.
  • The accelerated phase (AP) and blast crisis (BC) of CML are usually manifested by additionally acquired oncogene aberrations, resistance to therapy, advancing anaplasia, progressive organomegaly, and increased blast count.
  • Abnormal expression of some proto-oncogenes may accompany or even precede AP or BC of CML.
  • Our objective was to follow-up oncogene expression over time covering different clinical phases of CML.
  • Temporal variation in expression (percentage positivity per 1000 analyzed cells) of c-kit, c-myc, H-Ras, cyclin A1, p53, bcl-2 and VEGF oncogenic proteins in CP, AP, and BC of CML was studied by immunohistochemical procedures.
  • This was then correlated with parameters of clinical disease (organomegaly, duration of CP, AP, and BC) and laboratory (Hb, WBC and platelet counts, and the percentage of blasts) data.
  • The level of c-kit expression differed significantly over the course of disease (x(2), p = 0 x 025).
  • Antiapoptotic bcl-2 protein increased significantly with the progression of CML (x(2), p = 0 x 005).
  • There was no significant difference in the level of expression of H-Ras, cyclin A1 and p53 over the course of disease.
  • CONCLUSION: The changes in oncogene expression, assessed by immunohistochemical approach over the course of CML may have clinical relevance in deciding on and timing of therapy.
  • Temporal distribution of changes in oncoprotein expression in CML requires further study at the molecular level.
  • [MeSH-major] Blast Crisis / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. Proto-Oncogene Proteins c-myc / metabolism



91. Quintas-Cardama A, Kantarjian H, Talpaz M, O'Brien S, Garcia-Manero G, Verstovsek S, Rios MB, Hayes K, Glassman A, Bekele BN, Zhou X, Cortes J: Imatinib mesylate therapy may overcome the poor prognostic significance of deletions of derivative chromosome 9 in patients with chronic myelogenous leukemia. Blood; 2005 Mar 15;105(6):2281-6
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  • [Title] Imatinib mesylate therapy may overcome the poor prognostic significance of deletions of derivative chromosome 9 in patients with chronic myelogenous leukemia.
  • Deletions of derivative chromosome 9 [der(9)] can be identified by fluorescence in situ hybridization (FISH) in 10% to 15% of patients with chronic myeloid leukemia (CML).
  • We investigated the frequency and prognostic significance of der(9) deletions among 352 patients with CML treated with imatinib mesylate at our institution, in whom a deletion status of der(9) was determined.
  • Thirty-three patients (9%; 95% CI 0.07, 0.13) (30 in chronic phase, 3 in accelerated phase) had der(9) deletions.
  • In a multivariate analysis, der(9) deletions had no significant impact on response, survival, or response duration.
  • We conclude that treatment with imatinib mesylate overcomes the adverse prognostic significance of der(9) deletions in patients with CML.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Chromosome Deletion. Chromosomes, Human, Pair 9. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Adolescent. Adult. Aged. Benzamides. Disease-Free Survival. Female. Follow-Up Studies. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Interferons / administration & dosage. Interferons / adverse effects. Male. Middle Aged. Remission Induction. Treatment Outcome

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  • (PMID = 15572595.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; 9008-11-1 / Interferons
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92. Conte E, Stagno F, Guglielmo P, Scuto A, Consoli C, Messina A: Survivin expression in chronic myeloid leukemia. Cancer Lett; 2005 Jul 8;225(1):105-10
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  • [Title] Survivin expression in chronic myeloid leukemia.
  • In this study, we investigated the expression of survivin (SVV) in 44 patients with typical Ph-positive chronic myeloid leukemia (CML) in different phases of the disease as well as in 20 matched healthy donors.
  • We found a very high SVV expression in a predominant percentage of CML patients.
  • We also observed a significantly increased SVV expression in patients in accelerated/blastic phase of the disease compared to patients in chronic phase.
  • Moreover, SVV expression levels correlated in all CML patients with % of Ph-chromosome positive cells, with Bcr-Abl expression levels and with WBC-count.
  • Based on this finding we suggest that SVV detection and monitoring in CML could represent both a useful biomarker and attractive candidate for devising new targeted and combined therapies in CML.
  • [MeSH-major] Biomarkers, Tumor / blood. Gene Expression Profiling. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Microtubule-Associated Proteins / biosynthesis. Microtubule-Associated Proteins / blood

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  • (PMID = 15922862.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
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93. Talpaz M, Shah NP, Kantarjian H, Donato N, Nicoll J, Paquette R, Cortes J, O'Brien S, Nicaise C, Bleickardt E, Blackwood-Chirchir MA, Iyer V, Chen TT, Huang F, Decillis AP, Sawyers CL: Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias. N Engl J Med; 2006 Jun 15;354(24):2531-41
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  • [Title] Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias.
  • BACKGROUND: The BCR-ABL tyrosine kinase inhibitor imatinib is effective in Philadelphia chromosome-positive (Ph-positive) leukemias, but relapse occurs, mainly as a result of the outgrowth of leukemic subclones with imatinib-resistant BCR-ABL mutations.
  • We evaluated dasatinib, a BCR-ABL inhibitor that targets most imatinib-resistant BCR-ABL mutations, in patients with chronic myelogenous leukemia (CML) or Ph-positive acute lymphoblastic leukemia (ALL).
  • METHODS: Patients with various phases of CML or with Ph-positive ALL who could not tolerate or were resistant to imatinib were enrolled in a phase 1 dose-escalation study.
  • RESULTS: A complete hematologic response was achieved in 37 of 40 patients with chronic-phase CML, and major hematologic responses were seen in 31 of 44 patients with accelerated-phase CML, CML with blast crisis, or Ph-positive ALL.
  • Responses were maintained in 95 percent of patients with chronic-phase disease and in 82 percent of patients with accelerated-phase disease, with a median follow-up more than 12 months and 5 months, respectively.
  • Nearly all patients with lymphoid blast crisis and Ph-positive ALL had a relapse within six months.
  • Responses occurred among all BCR-ABL genotypes, with the exception of the T315I mutation, which confers resistance to both dasatinib and imatinib in vitro.
  • CONCLUSIONS: Dasatinib induces hematologic and cytogenetic responses in patients with CML or Ph-positive ALL who cannot tolerate or are resistant to imatinib. (ClinicalTrials.gov number, NCT00064233 [ClinicalTrials.gov].).
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Fusion Proteins, bcr-abl / antagonists & inhibitors. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Thiazoles / administration & dosage

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  • [Copyright] Copyright 2006 Massachusetts Medical Society.
  • [CommentIn] N Engl J Med. 2006 Sep 7;355(10):1062; author reply 1063-4 [16957155.001]
  • [CommentIn] N Engl J Med. 2006 Jun 15;354(24):2594-6 [16775240.001]
  • [CommentIn] N Engl J Med. 2006 Sep 7;355(10):1062-3; author reply 1063-4 [16960978.001]
  • (PMID = 16775234.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00064233
  • [Grant] United States / NCRR NIH HHS / RR / M01-RR-00865
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
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94. Kim YR, Cho HI, Yoon SS, Park S, Kim BK, Lee YK, Chun H, Kim HC, Lee DS: Interpretation of submicroscopic deletions of the BCR or ABL gene should not depend on extra signal-FISH: problems in interpretation of submicroscopic deletion of the BCR or ABL gene with extra signal-FISH. Genes Chromosomes Cancer; 2005 May;43(1):37-44
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  • [Title] Interpretation of submicroscopic deletions of the BCR or ABL gene should not depend on extra signal-FISH: problems in interpretation of submicroscopic deletion of the BCR or ABL gene with extra signal-FISH.
  • Several groups have demonstrated that a submicroscopic gene deletion in Ph+ chronic myelogenous leukemia (CML) is associated with a poor prognosis and reduced response to treatment.
  • To assess the variation between detection methods in the interpretation of a submicroscopic gene deletion, we performed an extra signal (ES)-FISH BCR/ABL and double-FISH (D-FISH) BCR/ABL on frozen bone marrow cells from 79 patients with CML (63 in the chronic phase, 6 in the accelerated phase, and 10 in blast crisis) and 30 patients with a BCR/ABL-negative myeloproliferative disorder as determined by RT-PCR.
  • The cutoff values for false-positive signals from a juxtaposition of the BCR and ABL gene were 11% in ES-FISH and 13% in D-FISH.
  • Of the 14 patients who showed an ABL gene deletion by ES-FISH, 5 had an ABL deletion only, 5 had both a BCR and an ABL deletion, but 4 proved to have a classic BCR/ABL rearrangement without a submicroscopic deletion, as determined by D-FISH.
  • Discrepant results between ES- and D-FISH were observed in 12 of the 79 patients (15.8%), and the main causes of a discrepancy were a false-positive ABL deletion (4 of 12, 33%), a variant Philadelphia chromosome (3 of 12, 25%), an inversion of derivative chromosome 9 at the very breakpoint of the ABL gene (9q32) (1 of 12, 8.3%), a cryptic variant Ph chromosome (1 of 12, 8.3%), and a marker chromosome (1 of 12, 8.3%).
  • Although there was no significant difference in the sensitivity for the detection of the fusion signal between ES- and D-FISH, ES-FISH showed a high percentage of cells with false-positive fusion signals (1 orange, 1 green, 1 yellow), which makes it difficult to interpret the submicroscopic ABL deletion.
  • In conclusion, an interpretation of the submicroscopic deletions of the BCR or ABL gene should not depend on ES-FISH.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Gene Deletion. Genes, abl. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Bone Marrow / pathology. Humans. In Situ Hybridization, Fluorescence. Prognosis. Proto-Oncogene Proteins c-bcr. Reproducibility of Results. Reverse Transcriptase Polymerase Chain Reaction. Sensitivity and Specificity

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15723338.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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95. 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



96. 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



97. 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



98. 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



99. 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



100. Sessions J: Chronic myeloid leukemia in 2007. Am J Health Syst Pharm; 2007 Dec 15;64(24 Suppl 15):S4-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic myeloid leukemia in 2007.
  • PURPOSE: Chronic myeloid leukemia (CML), a hematopoietic stem cell cancer representing 15-20% of adult leukemias, is discussed.
  • SUMMARY: CML is a myeloproliferative disorder that affects all lineages of hematopoiesis.
  • Final confirmation of CML comes with detection of the Philadelphia Chromosome (Ph) or BCR-ABL transcripts.
  • The disease presents in one of three phases: chronic phase, accelerated phase, or blast crisis.
  • Progression from chronic phase to accelerated phase usually involves the accumulation of additional cytogenetic aberrations and the arising