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

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  • [ErratumIn] Cancer. 2007 Jun 15;109(12):2625. Dosage error in article text
  • (PMID = 17154172.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Benzamides; 0 / Harringtonines; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 6FG8041S5B / homoharringtonine; 8A1O1M485B / Imatinib Mesylate
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2. Irfan SM, Bhurgri Y: Clinico-pathological features and outcomes in chronic phase chronic myeloid leukemia patients treated with hydroxyurea. Asian Pac J Cancer Prev; 2009 Oct-Dec;10(4):591-4
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  • [Title] Clinico-pathological features and outcomes in chronic phase chronic myeloid leukemia patients treated with hydroxyurea.
  • OBJECTIVE: To study the clinico-pathological features and major outcomes in patients with chronic myeloid leukemia, chronic phase, treated with hydroxyurea.
  • The median age at diagnosis was 39 years (range 11 to 66 years).
  • The median delay in diagnosis was 156 days (range 30 to 360 days).
  • LDH values above 1,000 ug/l were observed in 38 (21.5%) cases and creatinine above 1.5 ug/l in 21 (12%) cases.
  • All patients tested, were positive for Philadelphia chromosome and bcr-abl transcripts.
  • At the close of the study, disease advancement was observed in 76 (43.2%) cases, of which 35 (20%) transformed to acute leukemia.
  • One hundred and two (58.4%) patients were in chronic phase, 22 (12.5%) in accelerated phase and 19 (10.7%) in blast crisis.
  • Disease progression remained the major cause of death and was seen in 29 (16.4%) patients.
  • CONCLUSION: In the study population, CML was observed in a younger age group with significant delay in definitive diagnosis.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hydroxyurea / therapeutic use. Leukemia, Myeloid, Chronic-Phase / drug therapy. Leukemia, Myeloid, Chronic-Phase / pathology



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

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  • (PMID = 18321570.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Blood Glucose; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
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4. 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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5. Weisser M, Tischer J, Schnittger S, Schoch C, Ledderose G, Kolb HJ: A comparison of donor lymphocyte infusions or imatinib mesylate for patients with chronic myelogenous leukemia who have relapsed after allogeneic stem cell transplantation. Haematologica; 2006 May;91(5):663-6
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  • [Title] A comparison of donor lymphocyte infusions or imatinib mesylate for patients with chronic myelogenous leukemia who have relapsed after allogeneic stem cell transplantation.
  • Imatinib mesylate is highly effective in relapsed chronic myelogenous leukemia (CML) after allogeneic hematopoetic stem cell transplantation (HSCT).
  • The outcome of CML patients transplanted at our center who had received only imatinib for relapse after HSCT was compared with that of patients treated with donor lymphocyte infusions (DLI).
  • Imatinib therapy resulted in a higher incidence of relapse and inferior leukemia-free survival (p=0.006 and p=0.016, respectively).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Lymphocyte Transfusion. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Salvage Therapy
  • [MeSH-minor] Adult. Benzamides. Biomarkers, Tumor / biosynthesis. Disease-Free Survival. Female. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / biosynthesis. Humans. Imatinib Mesylate. Leukemia, Myeloid, Accelerated Phase / surgery. Leukemia, Myeloid, Chronic-Phase / surgery. Living Donors. Male. Middle Aged. Recurrence. Remission Induction. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 16627251.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Biomarkers, Tumor; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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6. Olivieri A, Manzione L: Dasatinib: a new step in molecular target therapy. Ann Oncol; 2007 Jun;18 Suppl 6:vi42-6
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  • The chimeric BCR-ABL gene, originated by the Philadelphia chromosome, encodes a fusion protein, BCR-ABL, bearing unregulated tyrosine kinase activity, the pivotal pathogenetic step of chronic myeloid leukemia (CML).
  • Imatinib, an inhibitor of the BCR-ABL tyrosine kinase, significantly improves the outcome of patients with CML.
  • Although the majority of CML patients are responsive to imatinib, a subset of patients loses the response and some progress to accelerated- or blast-phase CML.
  • The understanding of mechanisms of imatinib resistance has led to the development of novel BCR-ABL inhibitors; among these, dasatinib emerged as the most promising, being approximately 300-fold more potent than imatinib; it also inhibits SRC family kinases.
  • Preliminary data, after the introduction of dasatinib in clinical trials, in patients with CML, suggest that this drug is safe and well tolerated; furthermore, the majority of patients with imatinib-resistant disease achieved objective responses, although the durability of responses remains to be defined.
  • The preclinical data concerning its activity on several human solid tumor lines widen new opportunities for their use outside CML.

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  • (PMID = 17591830.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
  • [Number-of-references] 30
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7. 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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  • [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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8. 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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9. Michor F: Chronic myeloid leukemia blast crisis arises from progenitors. Stem Cells; 2007 May;25(5):1114-8
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  • [Title] Chronic myeloid leukemia blast crisis arises from progenitors.
  • Chronic myeloid leukemia (CML) progresses through three distinct clinical stages: chronic phase, accelerated phase, and blast crisis.
  • The progression to accelerated phase and blast crisis is driven by activation of oncogenes, inactivation of tumor suppressor genes, and/or amplification of the BCR-ABL fusion gene, which causes the chronic phase of the disease.
  • Here, I develop a simple mathematical model of CML blast crisis to investigate whether blasts arise from leukemic stem cells or more differentiated leukemic cells.
  • Therefore, CML blasts are likely to arise from leukemic progenitors.
  • [MeSH-major] Blast Crisis / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Benzamides. Disease Progression. Humans. Imatinib Mesylate. Models, Immunological. Mutation. Piperazines / therapeutic use. Pyrimidines / therapeutic use



10. Wallen H, Gooley TA, Deeg HJ, Pagel JM, Press OW, Appelbaum FR, Storb R, Gopal AK: Ablative allogeneic hematopoietic cell transplantation in adults 60 years of age and older. J Clin Oncol; 2005 May 20;23(15):3439-46
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  • Diagnoses included myelodysplastic syndrome (MDS; n = 35), chronic myeloid leukemia (CML; n = 8), acute myeloid leukemia (AML; n = 6), and other (n = 3).
  • Grade 3 to 4 acute graft-versus-host disease (GVHD) occurred in 20% of patients, and chronic extensive GVHD was described in 53% of patients.
  • Four of six patients with CML in chronic or accelerated phase are alive at a median of 6.9 years (range, 4.1 to 9.1 years) after transplantation.
  • None of the patients with AML, CML in blast crisis, or other diagnoses have survived.

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  • (PMID = 15824415.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / CA78902; United States / NHLBI NIH HHS / HL / HL 36444; United States / NCI NIH HHS / CA / T32 CA009515-20; United States / NCI NIH HHS / CA / CA15704; United States / NCI NIH HHS / CA / T32 CA009515; United States / NCI NIH HHS / CA / P01 CA1802; United States / NCI NIH HHS / CA / P01 CA078902
  • [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.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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11. 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



12. 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



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

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  • [Copyright] Copyright (c) 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 17503411.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA100067; United States / NCI NIH HHS / CA / CA105771; United States / NCI NIH HHS / CA / CA114395
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 3.1.3.16 / Protein Phosphatase 1; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6
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14. Babicka L, Zemanova Z, Pavlistova L, Brezinova J, Ransdorfova S, Houskova L, Moravcova J, Klamova H, Michalova K: Complex chromosomal rearrangements in patients with chronic myeloid leukemia. Cancer Genet Cytogenet; 2006 Jul 1;168(1):22-9
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  • [Title] Complex chromosomal rearrangements in patients with chronic myeloid leukemia.
  • During progression of chronic myeloid leukemia (CML) from the chronic to the accelerated phase and/or blast crisis, clonal evolution with nonrandom secondary aberrations such as +8, +Ph, i(17q), +19, -Y, +21, +17, and -7 is frequently observed.
  • The aim of this study was to determine the chromosomes and chromosomal regions which are involved in CCR during progression of the disease and the frequency of nonrandom changes.
  • Conventional cytogenetics, FISH, and multicolor FISH (mFISH) were used to study karyotypes of 18 CML patients with CCR ascertained by G-banding.
  • Precise determination of breakpoints involved in CCR can give new dimension to the understanding of genetic mechanisms which play role in progression of malignant disease.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Adult. Chromosome Banding. Chromosome Breakage / genetics. Chromosomes, Human, Pair 2 / genetics. Female. Fusion Proteins, bcr-abl / genetics. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Philadelphia Chromosome. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic



15. Akhlynina TV, Gerasimova LP, Sarkisian GP, Borovkova TV, Dukhovenskaia EA, Manakova TE, Naĭdenova NM, Timofeev AM, Grineva NI: [Kinetics of proliferation, differentiation and transcription of genes regulating apoptosis in cultured human BCR/ABL+ Ph+-cells]. Tsitologiia; 2007;49(10):889-900
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  • [Title] [Kinetics of proliferation, differentiation and transcription of genes regulating apoptosis in cultured human BCR/ABL+ Ph+-cells].
  • Ph+, bcr/abl+ cells arise due to t(9,22) chromosome translocation and Ph+ chromosome formation in hematopoietic stem cells.
  • Ph chromosome, bcr/abl oncogene and Ph+, bcr/abl+ cells themselves are the hallmark of chronic myeloid leukemia.
  • Under leukemia progression differentiating Ph+, bcr/abl+ cells transform into leukemic malignant cells with differentiation block.
  • This work was performed to develop a proper cell model allowing us to study functioning of differentiating Ph+, bcr/abl+ cells and their real transformation into malignant cells with block of differentiation.
  • For this purpose we have investigated kinetics of Ph+, bcr/abl+ cells proliferation, differentiation, cell death and transcription of antiapoptotic genes in cultured 14-day of Ph+ mononuclear cells isolated from peripheral blood of a patient in chronic phase of chronic myeloid leukemia before treatment.
  • The results obtained revealed that Ph+ cell differentiation proceeded in accord with characteristic scheme of chronic myeloid leukemia in vivo.
  • Myeloid cells of hematopoietic cell lineage amounted to 3/4 of live Ph+ mononuclear cells undergoing accumulation and subsequent consumption in the course of differentiation.
  • 95% myeloid cells were differentiating Ph+ granulocytes.
  • The peaks of antiapoptotic bcr/abl gene transcription activity coincided with the observed active proliferation at the beginning and at the end of cultivation.
  • Cell proliferation, differentiation and apoptosis were noticeably accelerated by growth factor treatment.
  • Thus, the study of the Ph+ cells cultivation kinetics is rather informative approach to investigation of continuous regulation of cellular and molecular processes in vitro in the case of chronic myeloid leukemia and allows more complete consideration of Ph+, bcr/abl+ cells hematopoiesis.
  • [MeSH-major] Apoptosis / genetics. Cell Differentiation / genetics. Cell Proliferation. Fusion Proteins, bcr-abl / genetics. Hematopoietic Stem Cells / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Philadelphia Chromosome

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  • (PMID = 18074781.001).
  • [ISSN] 0041-3771
  • [Journal-full-title] Tsitologiia
  • [ISO-abbreviation] Tsitologiia
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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16. Tam CS, Kantarjian H, Garcia-Manero G, Borthakur G, O'Brien S, Ravandi F, Shan J, Cortes J: Failure to achieve a major cytogenetic response by 12 months defines inadequate response in patients receiving nilotinib or dasatinib as second or subsequent line therapy for chronic myeloid leukemia. Blood; 2008 Aug 1;112(3):516-8
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  • [Title] Failure to achieve a major cytogenetic response by 12 months defines inadequate response in patients receiving nilotinib or dasatinib as second or subsequent line therapy for chronic myeloid leukemia.
  • Projected 1-year progression to hematologic failure, accelerated phase, or blast phase was also significantly different (3% vs 17%, P = .003).
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Pyrimidines / administration & dosage. Thiazoles / administration & dosage

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  • [Cites] Blood. 2001 Nov 15;98(10):3074-81 [11698293.001]
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  • (PMID = 18492956.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ PMC4082324
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17. Dutcher JP, Lee S, Gallagher RE, Makary AZ, Hines JD, Londer H, Farnen JP, Bennett JM, Paietta E, Rowe JM, Goloubeva O, Wiernik PH, Eastern Cooperative Oncology Group: Phase II study of all-trans retinoic acid in the accelerated phase or early blastic phase of chronic myeloid leukemia: a study of the Eastern Cooperative Oncology Group (E1993). Leuk Lymphoma; 2005 Mar;46(3):377-85
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  • [Title] Phase II study of all-trans retinoic acid in the accelerated phase or early blastic phase of chronic myeloid leukemia: a study of the Eastern Cooperative Oncology Group (E1993).
  • The aims of this study were to evaluate the safety and efficacy of all-trans retinoic acid (ATRA) in the treatment of the accelerated and blastic phase of chronic myeloid leukemia (CML) and to evaluate in vitro correlates of biological activity.
  • ATRA was administered in an intermittent schedule to patients with CML in the accelerated or blastic phases for a 6 week induction period, which was continued if there was evidence of clinical response or stable disease.
  • Laboratory correlative studies were performed prior to treatment and at intervals during treatment to evaluate effects on maturation and differentiation, and on CML progenitor cell growth by assessment of colony-forming cells (CFC).
  • ATRA demonstrated clinical and hematological activity in 5 of 18 patients with the accelerated phase of CML, and there was evidence of a biological effect in laboratory studies of 3 of the 5 patients' progenitor cells.
  • Combination therapy with other differentiating agents may be useful in this disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Tretinoin / administration & dosage
  • [MeSH-minor] Adult. Aged. Blast Crisis. Combined Modality Therapy. Cytogenetic Analysis. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Interferon-alpha / administration & dosage. Interferon-alpha / adverse effects. Male. Middle Aged. Recombinant Proteins. Survival Analysis. Time Factors

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  • (PMID = 15621827.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 11083; United States / NCI NIH HHS / CA / CA 14548; United States / NCI NIH HHS / CA / CA 14958; United States / NCI NIH HHS / CA / CA 23318; United States / NCI NIH HHS / CA / CA 66636; United States / NCI NIH HHS / CA / CA21115
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Recombinant Proteins; 5688UTC01R / Tretinoin; 76543-88-9 / interferon alfa-2a
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18. Yeh CH, Tseng R, Zhang Z, Cortes J, O'Brien S, Giles F, Hannah A, Estrov Z, Keating M, Kantarjian H, Albitar M: Circulating heat shock protein 70 and progression in patients with chronic myeloid leukemia. Leuk Res; 2009 Feb;33(2):212-7
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  • [Title] Circulating heat shock protein 70 and progression in patients with chronic myeloid leukemia.
  • We evaluated the association of circulating levels of heat shock protein 70 (Hsp70) in plasma with clinical behavior and progression in 139 chronic myeloid leukemia (CML) patients.
  • Circulating Hsp70 levels did not differ significantly between CML patients in the chronic phase (n=93; median 33.24 ng/mL, range 3.89-128.2 ng/mL) and those in the accelerated/blast phase (n=46; median 26.57 ng/mL, range 4.5-114.7 ng/mL).
  • However, overall CML patients had significantly higher levels of Hsp70 than healthy subjects (n=95, median 4.17 ng/mL, range 1.75-24.7 ng/mL) (P<0.001).
  • In chronic phase CML patients, Hsp70 levels above the median were associated with a higher rate of progression to the accelerated/blast phase and a tendency toward shorter survival.
  • Plasma Hsp70 thus could be a potential marker for predicting disease progression in patients with chronic phase CML.
  • [MeSH-major] HSP70 Heat-Shock Proteins / blood. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Benzamides. Biomarkers / blood. Disease Progression. Humans. Imatinib Mesylate. Leukemia, Myeloid, Accelerated Phase / diagnosis. Leukemia, Myeloid, Chronic-Phase / diagnosis. Middle Aged. Piperazines / therapeutic use. Prognosis. Pyrimidines / therapeutic use. Young Adult

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  • [CommentIn] Leuk Res. 2009 Feb;33(2):205-6 [18752847.001]
  • (PMID = 18715642.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Biomarkers; 0 / HSP70 Heat-Shock Proteins; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ NIHMS593155; NLM/ PMC4163801
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19. Wodarz D: Stem cell regulation and the development of blast crisis in chronic myeloid leukemia: Implications for the outcome of Imatinib treatment and discontinuation. Med Hypotheses; 2008;70(1):128-36
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  • [Title] Stem cell regulation and the development of blast crisis in chronic myeloid leukemia: Implications for the outcome of Imatinib treatment and discontinuation.
  • Chronic myeloid leukemia (CML) is a cancer of the hematopoietic system that is initiated by a single genetic alteration (the BCR-ABL fusion gene or Philadelphia chromosome) and progresses in several phases: during the chronic phase the number of cells grows slowly and the fraction of immature cells is low.
  • During the accelerated phase and blast crisis, the population of CML cells and the fraction of immature cells rises sharply.
  • The mechanisms that drive the transition from the chronic phase to blast crisis are not understood, and the requirement of genetic instability and further mutations has been suggested.
  • Using mathematical models, I describe a theory that can account for the transition from the chronic phase to blast crisis without the need to invoke further mutations.
  • According to the model, treatment can lead to the low level persistence of CML stem cells without assuming that these cells are less susceptible to drug-mediated activity, and this might explain why disease tends to relapse after treatment discontinuation even in the absence of acquired drug resistance.
  • Further, the model defines conditions when Imatinib treatment might lead to the eradication of CML, which is relevant in the context of recent data that show absence of relapse as long as two years after treatment cessation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blast Crisis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Cell Division / drug effects. Disease Progression. Drug Administration Schedule. Humans. Imatinib Mesylate. Models, Biological. Stem Cells / pathology



20. Wang GR, Zhao YZ, Qian LS, Zou DH, Li R, Mi YC, Wang XX, Qiu LG: [Analysis of long-term treatment outcome and related factors in 95 chronic myeloid leukemia patients treated with imatinib]. Zhonghua Xue Ye Xue Za Zhi; 2008 Jan;29(1):18-22
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  • [Title] [Analysis of long-term treatment outcome and related factors in 95 chronic myeloid leukemia patients treated with imatinib].
  • OBJECTIVE: To investigate the efficacy of imatinib in the treatment of chronic myeloid leukemia (CML) and analyse the treatment outcome and related factors.
  • METHODS: Ninety five CML patients were treated with imatinib in our hospital from May 2002 to May 2006.
  • (1) One year after therapy, there were 95.5% of chronic phase (CP) patients achieved complete hematologic response (CHR).
  • The expected survival at 12-, 24-, 36- and 50-month after imatinib treatment for CP group was (98.1 +/-1.9)%, (87.8 +/- 7.1)%, (81.9 +/- 8.7)% and (81.9 +/- 8.7)%, respectively. (2) Twelve month after therapy, there are 70% of accelerated phase (AP) patients achieve CHR and 10% get MCyR.
  • Conclusion (1) Imatinib as a primary treatment for CP CML can significantly improve the survival time as compared with that AP or BC patients or with that used in previously treated patients. (2) Imatinib could induce hematologic, even cytogenetic response to a certain extent, in CP or BC patients and prolong the survival time.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use



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

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  • [Copyright] 2010 Massachusetts Medical Society
  • [CommentIn] N Engl J Med. 2010 Jun 17;362(24):2314-5 [20525994.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1672; author reply 1673-5 [20961253.001]
  • [CommentIn] Expert Opin Pharmacother. 2011 Jan;12(1):157-63 [21108601.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1673; author reply 1673-5 [20973146.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1673; author reply 1673-5 [20973145.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1672-3; author reply 1673-5 [20973144.001]
  • (PMID = 20525993.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00471497
  • [Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Investigator] Moiraghi B; Perez M; Greil R; Valent P; Bosly A; Martiat P; Noens L; André M; Verhoef G; Conchon M; Souza C; Nonino A; Hungria V; Zanichelli MA; Colturato V; Forrest D; Lipton JH; Savoie ML; Delage R; Lalancette M; Quintero G; Gomez M; Klamova H; Faber E; Bjerrum OW; Fredriksen H; Vestergaard H; Marcher C; Kamel H; Elzawam H; Porkka K; Remes K; Reiffers J; Guilhot F; Facon T; Tulliez M; Guerci-Bresler AP; Nicolini FE; Charbonnier A; Rea D; Johnson-Ansah A; Legros L; Harousseau JL; Rigal-Huguet F; Escoffre M; Gardembas M; Guyotat D; Cahn JY; Gattermann N; Ottmann O; Niederwieser D; Stegelmann F; Schafhausen P; Brümmendorf T; Duyster J; Blumenstengel K; Scheid C; Kneba M; Kwong YL; Masszi T; Petrini M; Alimena G; Di Raimondo F; Rosti G; Rotoli B; Pane F; Pungolino E; Amadori S; Abruzzese E; Fioritoni G; Lauria F; Bosi A; Martelli M; Rambaldi A; Ferrara F; Nobile F; Gobbi M; Carella AM; Orlandi EM; Leoni P; Tiribelli M; Levis A; Imamura M; Takahashi N; Tsukamoto N; Chiba S; Nagai T; Okamoto S; Miura O; Kurokawa M; Ohnishi K; Toba K; Nakao S; Tomita A; Miyamura K; Hino M; Maeda Y; Kimura A; Kawaguchi T; Miyazaki Y; Nakaseko C; Jinnai I; Matsuda A; Matsumura I; Ishikawa J; Ohyashiki K; Okada M; Usuki K; Kobayashi Y; Ohishi K; Imai K; Miyawaki S; Kanda Y; Park SY; Kim HJ; Sohn SK; Lee KH; Jung CW; Ong TC; Gómez Almaguer D; Kassack J; Ossenkoppele GJ; Gedde-Dahl T; Hjorth-Hansen H; Jedrzejczak W; Dmoszynska A; Starzak-Dwozdz J; Holowiecki J; Kyrcz-Krzemieñ S; Kuliczkowski K; Zaritsky A; Turkina A; Pospelova T; Goh YT; Koh LP; Demitrovicova L; Mistrik M; Ruff P; Louw V; Dreosti LM; Novitzky N; Cohen G; Cervantes F; Cañizo C; de Paz R; del Castillo S; Perez Encinas M; Sanz Alonso M; Marin F; Pérez-López R; Hernandez Boluda J; Echeveste Gutierrez MA; Odriozola J; Herrera P; Steegman JL; Conde E; Lopez P; Giraldo P; Boque C; Heredia B; Font AJ; Rodriguez RF; Rodriguez MJ; Batlle J; Stenke L; Lehmann S; Wadenvik H; Simonsson B; Markevärn B; Själander A; Richter J; Bjoreman M; Eriksson KM; Chalandon Y; Shih LY; Yao M; Wang MC; Jootar S; Bunworasate U; Ulkü B; Haznedar R; Undar B; Sahin B; Marin D; Smith G; Byrne J; Holyoake T; Kalaycio M; Akard L; Heaney M; Al-Janadi A; Goldberg S; Powell B; Harker WG; Shea T; Gingrich R; Glass J; Paquette R; Siegrist C; Woodson M; Fehrenbacher L; Koh H; Flinn I; Arrowsmith E; Ervin T; Guerra M; Wallach H; Berry W; Burke J; Edenfield W; Guzley G; Davis J; Richards D; Schlossman D; Kolibaba K; Alemany C; Savin M; Robbins G; Lopez J; Goldman JM; Camm J; Schiffer CA; Sargent DJ
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22. Zhu ZH, Qian J, Lin J, Qian Z, Yao DM, Wang YL, Chen Q, Xiao GF: [Quantification of prame gene transcript in chronic myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Aug;18(4):855-8
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  • [Title] [Quantification of prame gene transcript in chronic myeloid leukemia].
  • This study was purposed to analyze the expression level of preferentially expressed antigen of melanoma (prame) transcript in the patients with chronic myeloid leukemia (CML) and explore its clinical significance.
  • Real-time quantitative PCR (RQ-PCR) assay was used to detect the level of prame gene transcript in the bone marrow samples from 30 patients with CML and 15 patients with iron deficiency anemia (IDA).
  • The results showed that CML patients had significantly higher prame mRNA level (0% - 772.25%, median 8.28%) than IDA cases (0% - 1.46%, median 0.19%) (p < 0.001).
  • The level of prame gene transcript was significantly correlated with that of bcr-abl fusion gene transcript (r = 0.708, p < 0.001) in CML patients.
  • Furthermore, 6 patients in blastic crisis (BC) and accelerated phase (AP) had significantly higher prame gene transcript than that of 24 cases in chronic phase (CP) (p = 0.007).
  • In 2 CML patients with sequential samples, prame gene transcript increased in AP and BC, compared with in CP, and was consistent with the altering tendency of bcr-abl transcript.
  • It is concluded that the level of prame gene transcript increases in CML which associates with the progression of the disease, prame gene transcript level can be used for monitoring the disease state.



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



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



26. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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27. Wang XR, Kang HY, Cen J, Li YH, Wang LL, Yu L: [Methylation status of id4 gene promoter in patients with chronic myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Dec;18(6):1402-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Methylation status of id4 gene promoter in patients with chronic myeloid leukemia].
  • This study was purposed to investigate the methylation status of id4 gene promoter in patients with chronic myeloid leukemia (CML) and explore the relationship between methylation of the id4 gene and progress of CML.
  • The methylation status of id4 gene in 48 chronic myeloid leukemia patients and 10 healthy individuals was detected by using methylation-specific polymerase chain reaction (MS-PCR).
  • The results showed that id4 gene was unmethylated in bone marrow samples from both healthy individuals and CML patients in chronic phase (CP).
  • The rate of id4 gene methylation in both CML patients in accelerated phase (AP) and blast crisis (BC) was 66%, and was higher than those of CML patients in CP phase.
  • In one CML patient who received a serial observations, the status of id4 was unmethylated in CP, but it was methylated in AP and BC phase.
  • It is concluded that the id4 gene in CML patients is unmethylated in CP, while it is methylated in AP or BC.
  • The detection of id4 gene methylation status may be useful for monitoring disease advance in CML and may be used as a marker of disease progression in CML.

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  • (PMID = 21176338.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA Primers; 0 / ID4 protein, human; 0 / Inhibitor of Differentiation Proteins
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28. Mahon FX, Molimard M: Correlation between trough imatinib plasma concentration and clinical response in chronic myeloid leukemia. Leuk Res; 2009 Aug;33(8):1147-8; author reply 1149-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Correlation between trough imatinib plasma concentration and clinical response in chronic myeloid leukemia.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / pharmacokinetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / administration & dosage. Piperazines / pharmacokinetics. Pyrimidines / administration & dosage. Pyrimidines / pharmacokinetics
  • [MeSH-minor] Benzamides. Cytogenetic Analysis. Drug Monitoring. Female. Fusion Proteins, bcr-abl / analysis. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Leukemia, Myeloid, Accelerated Phase. Leukemia, Myeloid, Chronic-Phase. Male. Middle Aged. Polymerase Chain Reaction. Risk Assessment

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  • [CommentOn] Leuk Res. 2009 Feb;33(2):271-5 [18762338.001]
  • (PMID = 19395027.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comment; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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29. Gratwohl A, Heim D: Current role of stem cell transplantation in chronic myeloid leukaemia. Best Pract Res Clin Haematol; 2009 Sep;22(3):431-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current role of stem cell transplantation in chronic myeloid leukaemia.
  • Haematopoietic stem cell transplantation (HSCT) has seen considerable ups and downs in its role for patients with chronic myeloid leukaemia (CML).
  • It has provided the first proof of the principle for cure and has confirmed the concept of successful immunotherapy of leukaemia.
  • CML became the most frequent indication for an allogeneic HSCT worldwide.
  • The frequency of HSCT declined rapidly when the specific BCR/ABL tyrosine kinase inhibitor (TKI) imatinib appeared.
  • Risk assessment of both, disease risk and transplant risk, has become standard.
  • Allogeneic HSCT remains the first-line approach for patients with CML in accelerated phase or blast crisis.
  • It is the best option for all patients with failed second-line TKIs, with mutations T315I or with progressive disease.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Protein Kinase Inhibitors / therapeutic use

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  • (PMID = 19959092.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors
  • [Number-of-references] 74
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30. Fausel CA: Novel treatment strategies for chronic myeloid leukemia. Am J Health Syst Pharm; 2006 Dec 1;63(23 Suppl 8):S15-20; quiz S21-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel treatment strategies for chronic myeloid leukemia.
  • PURPOSE: Despite dramatic advances in the treatment of chronic myeloid leukemia (CML), resistance to therapeutic agents has emerged as a significant treatment dilemma.
  • Mutations of the BCR-ABL kinase domain, a common mechanism of resistance to imatinib in CML, are discussed.
  • SUMMARY: Several new targeted kinase inhibitors have reached clinical trials and have proved to be efficacious in halting the oncogenic activity of most BCR-ABL mutants.
  • Dasatinib is 300 times more potent than imatinib at BCR-ABL inhibition, has few side effects, and inhibits the SRC family kinases.
  • Nilotinib inhibits BCR-ABL at 20-50 times more potency than imatinib.
  • Both agents were highly effective in treating chronic phase CML but were less effective at treating accelerated phase CML in early phase clinical trials.
  • CONCLUSION: The new kinase inhibitors, dasatinib and nilotinib, are emerging as plausible therapeutic options for the treatment of imatinib-refractory CML.
  • [MeSH-major] Drug Therapy / methods. Immunotherapy, Active / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy



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



32. Terasawa T, Dahabreh I, Trikalinos TA: BCR-ABL mutation testing to predict response to tyrosine kinase inhibitors in patients with chronic myeloid leukemia. PLoS Curr; 2010 Dec 07;2:RRN1204
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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 mutation testing to predict response to tyrosine kinase inhibitors in patients with chronic myeloid leukemia.
  • Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment of chronic myeloid leukemia (CML).
  • Although randomized evidence demonstrates that imatinib (a commercially available TKI) prolongs event-free survival in patients with CML, some patients develop imatinib intolerance or resistance.
  • In addition, imatinib is less effective in patients who have progressed to more advanced disease stages, such as accelerated phase and blastic phase CML.
  • For these reasons, 2nd generation TKIs that can inhibit the BCR-ABL protein more effectively or target additional disease mechanisms have been developed.
  • Resistance to TKI treatment is thought to be mediated through various mechanisms, the most common of which is BCR-ABL1 mutations.
  • Testing for mutations in BCR-ABL1 may predict lack of response to imatinib or may inform the choice between alternative TKIs.

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  • (PMID = 21188137.001).
  • [ISSN] 2157-3999
  • [Journal-full-title] PLoS currents
  • [ISO-abbreviation] PLoS Curr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3001986.1
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33. le Coutre P, Ottmann OG, Giles F, Kim DW, Cortes J, Gattermann N, Apperley JF, Larson RA, Abruzzese E, O'Brien SG, Kuliczkowski K, Hochhaus A, Mahon FX, Saglio G, Gobbi M, Kwong YL, Baccarani M, Hughes T, Martinelli G, Radich JP, Zheng M, Shou Y, Kantarjian H: Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is active in patients with imatinib-resistant or -intolerant accelerated-phase chronic myelogenous leukemia. Blood; 2008 Feb 15;111(4):1834-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is active in patients with imatinib-resistant or -intolerant accelerated-phase chronic myelogenous leukemia.
  • Patients with imatinib-resistant or -intolerant accelerated-phase chronic myelogenous leukemia (CML-AP) have very limited therapeutic options.
  • Nilotinib is a highly selective BCR-ABL tyrosine kinase inhibitor.
  • This phase 2 trial was designed to characterize the efficacy and safety of nilotinib (400 mg twice daily) in this patient population with hematologic response (HR) as primary efficacy endpoint.
  • In conclusion, nilotinib is an effective and well-tolerated treatment in imatinib-resistant and -intolerant CML-AP.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / genetics. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Aged. Benzamides. Blood Cell Count. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Resistance. Female. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Male. Middle Aged. Mutation. Safety

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  • (PMID = 18048643.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00384228
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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34. 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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  • (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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35. Remsing Rix LL, Rix U, Colinge J, Hantschel O, Bennett KL, Stranzl T, Müller A, Baumgartner C, Valent P, Augustin M, Till JH, Superti-Furga G: Global target profile of the kinase inhibitor bosutinib in primary chronic myeloid leukemia cells. Leukemia; 2009 Mar;23(3):477-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Global target profile of the kinase inhibitor bosutinib in primary chronic myeloid leukemia cells.
  • The detailed molecular mechanism of action of second-generation BCR-ABL tyrosine kinase inhibitors, including perturbed targets and pathways, should contribute to rationalized therapy in chronic myeloid leukemia (CML) or in other affected diseases.
  • Here, we characterized the target profile of the dual SRC/ABL inhibitor bosutinib employing a two-tiered approach using chemical proteomics to identify natural binders in whole cell lysates of primary CML and K562 cells in parallel to in vitro kinase assays against a large recombinant kinase panel.
  • The combined strategy resulted in a global survey of bosutinib targets comprised of over 45 novel tyrosine and serine/threonine kinases.
  • We have found clear differences in the target patterns of bosutinib in primary CML cells versus the K562 cell line.
  • Finally, bosutinib is the first kinase inhibitor shown to target CAMK2G, recently implicated in myeloid leukemia cell proliferation.
  • [MeSH-major] Aniline Compounds / pharmacology. Antineoplastic Agents / pharmacology. K562 Cells / drug effects. Leukemia, Myeloid, Accelerated Phase / enzymology. Neoplasm Proteins / antagonists & inhibitors. Nitriles / pharmacology. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Quinolines / pharmacology
  • [MeSH-minor] Calcium-Calmodulin-Dependent Protein Kinase Type 2 / antagonists & inhibitors. Dasatinib. Drug Delivery Systems. Drug Screening Assays, Antitumor. Fusion Proteins, bcr-abl / antagonists & inhibitors. Gene Expression Profiling. Humans. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / enzymology. Mitogen-Activated Protein Kinases / antagonists & inhibitors. Nerve Tissue Proteins / antagonists & inhibitors. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-abl / antagonists & inhibitors. Pyrimidines / pharmacology. Signal Transduction / drug effects. Substrate Specificity. Thiazoles / pharmacology. src-Family Kinases / antagonists & inhibitors



36. 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



37. 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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38. 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



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



41. Baron F, Maris MB, Storer BE, Sandmaier BM, Stuart MJ, McSweeney PA, Radich JP, Pulsipher MA, Agura ED, Chauncey TR, Maloney DG, Shizuru JA, Storb R: HLA-matched unrelated donor hematopoietic cell transplantation after nonmyeloablative conditioning for patients with chronic myeloid leukemia. Biol Blood Marrow Transplant; 2005 Apr;11(4):272-9
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  • [Title] HLA-matched unrelated donor hematopoietic cell transplantation after nonmyeloablative conditioning for patients with chronic myeloid leukemia.
  • We evaluated 10/10 HLA antigen-matched unrelated hematopoietic cell transplantation (HCT) after nonmyeloablative conditioning with fludarabine 3 x 30 mg/m2 and 2 Gy of total body irradiation as treatment for patients with chronic myeloid leukemia who were ineligible for conventional HCT.
  • Data from 21 consecutive patients in first chronic phase (CP1; n = 12), accelerated phase (AP; n = 5), second CP (CP2; n = 3), and blast crisis (n = 1) were analyzed.
  • The patient who underwent transplantation in blast crisis died on day 21 (too early to be evaluated for engraftment) from progressive disease.
  • Graft rejections were nonfatal in all cases and were followed by autologous reconstitution with persistence or recurrence of chronic myeloid leukemia.
  • Two of the remaining 4 patients died of nonrelapse causes in complete (n = 1) or major (n = 1) cytogenetic remissions, and 2 died of progressive disease.

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  • (PMID = 15812392.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA18029; United States / NCI NIH HHS / CA / CA78902; United States / NCI NIH HHS / CA / CA92058; United States / NCI NIH HHS / CA / CA49605; United States / NCI NIH HHS / CA / CA15704; United States / NCI NIH HHS / CA / P01 CA078902
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA Antigens
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42. DeAngelo DJ, Attar EC: Use of dasatinib and nilotinib in imatinib-resistant chronic myeloid leukemia: translating preclinical findings to clinical practice. Leuk Lymphoma; 2010 Mar;51(3):363-75
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  • [Title] Use of dasatinib and nilotinib in imatinib-resistant chronic myeloid leukemia: translating preclinical findings to clinical practice.
  • The BCR-ABL inhibitor imatinib revolutionized the treatment of chronic myeloid leukemia (CML).
  • The mechanisms underlying resistance are multifactorial and may include mutations in the kinase domain of BCR-ABL, increased production of BCR-ABL, or activation of BCR-ABL-independent pathways.
  • Two second-line BCR-ABL inhibitors are now approved for treatment of patients with resistance or intolerance to imatinib.
  • Dasatinib is a dual BCR-ABL/Src-family kinase (SFK) inhibitor approved for patients with imatinib-resistant and -intolerant CML in any phase and Ph+ ALL.
  • Nilotinib, an analogue of imatinib, is approved for the treatment of imatinib-resistant or -intolerant patients with chronic or accelerated phase CML.
  • Both agents have shown significant clinical activity in patients with imatinib-resistant or -intolerant CML, and their approval represents a major advancement in the treatment options available.
  • The presence of certain disease characteristics (e.g. specific BCR-ABL mutations) or patient comorbidities may facilitate more effective treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Mutation. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use



43. 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



44. 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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45. 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



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



47. Agis H, Krauth MT, Mosberger I, Müllauer L, Simonitsch-Klupp I, Schwartz LB, Printz D, Böhm A, Fritsch G, Horny HP, Valent P: Enumeration and immunohistochemical characterisation of bone marrow basophils in myeloproliferative disorders using the basophil specific monoclonal antibody 2D7. J Clin Pathol; 2006 Apr;59(4):396-402
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  • In chronic myeloid leukaemia (CML), basophilia is a diagnostic and prognostic determinant.
  • OBJECTIVE: To detect and enumerate basophils in bone marrow sections in patients with CML and other MPD.
  • METHODS: The anti-basophil antibody 2D7 was applied to paraffin embedded bone marrow sections from normal/reactive subjects (n = 31), patients with CML (chronic phase, n = 37; accelerated phase, n = 9), and other MPD (chronic idiopathic myelofibrosis (CIMF), n = 20; polycythaemia vera (PV), n = 20; essential thrombocythaemia (ET), n = 20; indolent systemic mastocytosis (ISM), n = 7).
  • 2D7(+) bone marrow cells were found to increase in CML compared with normal/reactive bone marrow and other MPD (median numbers of 2D7(+) cells/mm(2): CML, 33; normal/reactive bone marrow, 6; CIMF, 10; PV, 6; ET, 5; ISM, 3; p<0.05).
  • The highest basophil counts were recorded in accelerated phase CML (115/mm(2)).
  • This approach should help in the quantification of bone marrow basophils at diagnosis and during anti-leukaemic treatment.

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  • (PMID = 16461568.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI020487; United States / NIAID NIH HHS / AI / R21 AI020487; United States / NIAID NIH HHS / AI / R37 AI020487; United States / NIAID NIH HHS / AI / AI20487
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers; 820484N8I3 / Histamine
  • [Other-IDs] NLM/ PMC1860377
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48. 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



49. Valent P, Agis H, Sperr W, Sillaber C, Horny HP: Diagnostic and prognostic value of new biochemical and immunohistochemical parameters in chronic myeloid leukemia. Leuk Lymphoma; 2008 Apr;49(4):635-8
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  • [Title] Diagnostic and prognostic value of new biochemical and immunohistochemical parameters in chronic myeloid leukemia.
  • Chronic myeloid leukemia (CML) is a stem-cell disease characterized by multilineage expansion of clonal BCR/ABL+ cells.
  • Transformation from chronic into accelerated and blast phase of CML is usually associated with drug resistance and is accompanied by typical clinical and/or laboratory features, such as splenomegaly, increase in precursor cells, disturbed megakaryopoiesis, basophilia or marrow fibrosis.
  • Because of new treatment options, early recognition of disease-acceleration is of importance.
  • These tests are useful to quantitate basophil-lineage cells in the peripheral blood in CML, to determine and quantify basophilia in the bone marrow, and to detect focal accumulations of blast cells and megakaryocytes as well as increased angiogenesis and fibrosis in bone marrow sections.
  • Application of these markers may assist in determining the phase of disease and may help to better predict the prognosis in individual patients.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis



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



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

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  • (PMID = 19648168.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00006343
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Pyrimidines; 04079A1RDZ / Cytarabine; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC2791923
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52. Radich JP, Dai H, Mao M, Oehler V, Schelter J, Druker B, Sawyers C, Shah N, Stock W, Willman CL, Friend S, Linsley PS: Gene expression changes associated with progression and response in chronic myeloid leukemia. Proc Natl Acad Sci U S A; 2006 Feb 21;103(8):2794-9
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  • [Title] Gene expression changes associated with progression and response in chronic myeloid leukemia.
  • Chronic myeloid leukemia (CML) is a hematopoietic stem cell disease with distinct biological and clinical features.
  • The biologic basis of the stereotypical progression from chronic phase through accelerated phase to blast crisis is poorly understood.
  • We used DNA microarrays to compare gene expression in 91 cases of CML in chronic (42 cases), accelerated (17 cases), and blast phases (32 cases).
  • Three thousand genes were found to be significantly (P < 10(-10)) associated with phase of disease.
  • A comparison of the gene signatures of chronic, accelerated, and blast phases suggest that the progression of chronic phase CML to advanced phase (accelerated and blast crisis) CML is a two-step rather than a three-step process, with new gene expression changes occurring early in accelerated phase before the accumulation of increased numbers of leukemia blast cells.
  • Studies of CML patients who relapsed after initially successful treatment with imatinib demonstrated a gene expression pattern closely related to advanced phase disease.

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  • (PMID = 16477019.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE4170
  • [Grant] United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / CA-18029; United States / NCI NIH HHS / CA / CA-85053
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / DNA-Binding Proteins; 0 / Kruppel-Like Transcription Factors; 0 / MZF1 protein, human; 0 / Peptide Elongation Factor 1; 0 / Piperazines; 0 / Pyrimidines; 0 / Transcription Factors; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC1413797
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53. Landstrom AP, Knudson RA, Dewald GW, Ketterling RP, Tefferi A: Philadelphia chromosome mosaicism at diagnosis in chronic myeloid leukemia: clinical correlates and effect on imatinib mesylate treatment outcome. Leuk Lymphoma; 2007 Nov;48(11):2137-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Philadelphia chromosome mosaicism at diagnosis in chronic myeloid leukemia: clinical correlates and effect on imatinib mesylate treatment outcome.
  • In chemotherapy-treated patients with chronic myeloid leukemia (CML), the karyotypic detection of Philadelphia chromosome (Ph)-negative metaphases at diagnosis (i.e.
  • In the current retrospective study, clinical correlates and prognostic relevance of Ph mosaicism were evaluated in 63 Ph-positive patients with CML, including 59 in chronic phase and 4 in accelerated phase, receiving imatinib mesylate as either first (n = 46) or second (n = 17) line therapy.
  • Thirteen patients (21%) displayed Ph-negative metaphases at diagnosis and, compared to the other 50 patients with 100% Ph-positive metaphases, presented with significantly lower leukocyte count (p = 0.0004), circulating blast percentage (p = 0.02), and incidence of palpable splenomegaly (p = 0.02).
  • Ph mosaicism did not correlate with other CML-pertinent prognostic factors including Sokal score (p = 0.4) or the presence of additional chromosome changes (p = 0.96) found in 10 patients (16%).
  • Due to the small sample size, the current preliminary observations require validation in a larger group of patients.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Mosaicism. Philadelphia Chromosome. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 17926177.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / T32 GM072474
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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54. Wright MP, Shepherd JD, Barnett MJ, Nantel SH, Sutherland HJ, Toze CL, Hogge DE, Nevill TJ, Song KW, Abou Mourad YR, Narayanan S, Power MM, Smith CA, Forrest DL: Response to tyrosine kinase inhibitor therapy in patients with chronic myelogenous leukemia relapsing in chronic and advanced phase following allogeneic hematopoietic stem cell transplantation. Biol Blood Marrow Transplant; 2010 May;16(5):639-46
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  • [Title] Response to tyrosine kinase inhibitor therapy in patients with chronic myelogenous leukemia relapsing in chronic and advanced phase following allogeneic hematopoietic stem cell transplantation.
  • Tyrosine kinase inhibitors (TKI) have been used to treat relapse of chronic myelogenous leukemia (CML) after allogeneic stem cell transplant (HSCT), with responses seen predominantly in chronic phase (CP) patients.
  • This study aimed to analyze the response to TKI therapy and overall survival for patients relapsing predominantly in advanced phase.
  • We retrospectively reviewed 22 patients treated with imatinib (n=20) and/or dasatinib (n=6) for relapsed CML after HSCT; 8 patients were in CP, and 14 patients had advanced disease.
  • In advanced phase patients, 11 (79%) achieved CHR, 10 (71%) CCR, and 8 (57%) achieved CMR.
  • TKI therapy is capable of inducing durable molecular responses for CML relapsing after HSCT, both in chronic and advanced phases.
  • The achievement of CMR appears to be crucial in providing long-term disease control for these patients.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Protein Kinase Inhibitors / therapeutic use
  • [MeSH-minor] Adult. Female. Humans. Leukemia, Myeloid, Accelerated Phase / mortality. Leukemia, Myeloid, Accelerated Phase / therapy. Leukemia, Myeloid, Chronic-Phase / mortality. Leukemia, Myeloid, Chronic-Phase / therapy. Male. Middle Aged. Protein-Tyrosine Kinases / antagonists & inhibitors. Recurrence. Remission Induction. Retrospective Studies. Survival Rate. Transplantation, Homologous

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  • [Copyright] Copyright 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20005967.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases
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55. Verma D, Kantarjian H, Shan J, O'Brien S, Estrov Z, Garcia-Manero G, Koller C, Borthakur G, Cortes J: Survival outcomes for clonal evolution in chronic myeloid leukemia patients on second generation tyrosine kinase inhibitor therapy. Cancer; 2010 Jun 1;116(11):2673-81
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  • [Title] Survival outcomes for clonal evolution in chronic myeloid leukemia patients on second generation tyrosine kinase inhibitor therapy.
  • METHODS: The authors analyzed the outcome of 177 CML patients after second tyrosine kinase inhibitor therapy.
  • RESULTS: Ninety-five patients were in chronic phase, 30 had clonal evolution, 28 were in accelerated phase (AP), and 24 were in AP plus clonal evolution.
  • The hematologic and cytogenetic response rates, OS, and EFS were no different between patients in chronic phase with clonal evolution and patients with chronic phase and no clonal evolution.
  • The factors predicting increasing major cytogenetic response to second generation tyrosine kinase inhibitors were prior achievement of major cytogenetic response with imatinib, higher hemoglobin levels, no splenomegaly, lower percentage of Philadelphia chromosome-positive metaphases, and no prior chemotherapy.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / mortality. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use

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  • [Copyright] (c) 2010 American Cancer Society.
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  • (PMID = 20499401.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA049639; 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 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ NIHMS593644; NLM/ PMC4216809
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56. 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



57. Rodzaj M, Gałazka K, Majewski M, Zduńczyk A: A diagnostically difficult case of chronic myeloid neoplasm with eosinophilia and abnormalities of PDGFRA effectively treated with imatinib in accelerated phase: case report. Pol Arch Med Wewn; 2009 Dec;119(12):838-41
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  • [Title] A diagnostically difficult case of chronic myeloid neoplasm with eosinophilia and abnormalities of PDGFRA effectively treated with imatinib in accelerated phase: case report.
  • Chronic myeloid neoplasm with eosinophilia and abnormalities of platelet-derived growth factor receptor alpha (PDGFRA), referred to until 2008 as chronic eosinophilic leukemia, is distinguished from hypereosinophilic syndrome (HES), if accompanied by genetic abnormalities that enable to determine eosinophil clonality.
  • In chronic myeloid neoplasm with eosinophilia and abnormalities of PDGFRA the FIP1L1-PDGFRA fusion gene can be detected.
  • Differential diagnosis of HES is often difficult because hypereosinophilia may also be reactive and may occur in many nonhematological as well as hematological disorders.
  • Traditional treatment of chronic myeloid neoplasm with cytostatic drugs results in a short-term and transient remission or stabilization of the disease.
  • We present the case of a 52-year-old patient with chronic myeloid neoplasm with eosinophilia and abnormalities of PDGFRA, in whom acceleration occurred after a year of cytostatic therapy with hydroxyurea and was successfully treated with imatinib.
  • It was impossible to unequivocally determine the type of bone marrow disease based on histologic criteria, and a wide spectrum of molecular tests differentiating the type of myeloid proliferation were necessary to establish the diagnosis.
  • RT-PCR did not reveal BCR-ABL or JAK2 V617F mutation.
  • [MeSH-major] Hypereosinophilic Syndrome / diagnosis. Hypereosinophilic Syndrome / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Oncogene Proteins, Fusion / metabolism. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Receptor, Platelet-Derived Growth Factor alpha / metabolism. mRNA Cleavage and Polyadenylation Factors / metabolism
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Benzamides. Disease Progression. Gene Rearrangement. Humans. Imatinib Mesylate. Middle Aged. Protein Kinase Inhibitors / administration & dosage

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  • (PMID = 20010473.001).
  • [ISSN] 1897-9483
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / FIP1L1-PDGFRA fusion protein, human; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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58. Luk'ianova AS, Pien'kovs'ka-Hrelia B, Masliak ZV: [Complex cytogenetic aberrations in a patient with chronic myeloid leukemia: a case report]. Tsitol Genet; 2009 May-Jun;43(3):48-54
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  • [Title] [Complex cytogenetic aberrations in a patient with chronic myeloid leukemia: a case report].
  • In this article is presented a case of multiple chromosomal aberrations in a patient with CML accelerated phase.
  • Our data suggested that detected changes can be correlated with previous treatment regimens and the influence of these changes on progression of disease is discussed.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics



59. Palandri F, Castagnetti F, Alimena G, Testoni N, Breccia M, Luatti S, Rege-Cambrin G, Stagno F, Specchia G, Martino B, Levato L, Merante S, Liberati AM, Pane F, Saglio G, Alberti D, Martinelli G, Baccarani M, Rosti G: The long-term durability of cytogenetic responses in patients with accelerated phase chronic myeloid leukemia treated with imatinib 600 mg: the GIMEMA CML Working Party experience after a 7-year follow-up. Haematologica; 2009 Feb;94(2):205-12
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  • [Title] The long-term durability of cytogenetic responses in patients with accelerated phase chronic myeloid leukemia treated with imatinib 600 mg: the GIMEMA CML Working Party experience after a 7-year follow-up.
  • BACKGROUND: Imatinib mesylate is the first line treatment for chronic myeloid leukemia.
  • The advent of imatinib increased survival significantly in patients in an advanced phase of the disease.
  • DESIGN AND METHODS: A phase 2 multicenter trial of the use of imatinib 600 mg/daily in patients with accelerated phase chronic myeloid leukemia was sponsored and promoted by the Italian Cooperative Study Group on Chronic Myeloid Leukemia in 2001.
  • One hundred and seven patients (96%) returned to chronic phase and 79 patients (71%) achieved a complete hematologic response.
  • CONCLUSIONS: Imatinib may induce durable responses, associated with prolonged survival, in patients with accelerated phase chronic myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage

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  • (PMID = 19144656.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC2635408
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60. Jabbour E, Kantarjian H, Jones D, Talpaz M, Bekele N, O'Brien S, Zhou X, Luthra R, Garcia-Manero G, Giles F, Rios MB, Verstovsek S, Cortes J: Frequency and clinical significance of BCR-ABL mutations in patients with chronic myeloid leukemia treated with imatinib mesylate. Leukemia; 2006 Oct;20(10):1767-73
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  • [Title] Frequency and clinical significance of BCR-ABL mutations in patients with chronic myeloid leukemia treated with imatinib mesylate.
  • Mutations of the BCR-ABL kinase domain are a common mechanism of resistance to imatinib in chronic myeloid leukemia.
  • By multivariate analysis, factors associated with development of mutations were older age (P=0.026) prior interferon therapy (P=0.026), and accelerated phase or blast phase at time of imatinib failure (P=0.001).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. 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



61. 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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  • [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



62. 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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63. Perrotti D, Jamieson C, Goldman J, Skorski T: Chronic myeloid leukemia: mechanisms of blastic transformation. J Clin Invest; 2010 Jul;120(7):2254-64
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  • [Title] Chronic myeloid leukemia: mechanisms of blastic transformation.
  • The BCR-ABL1 oncoprotein transforms pluripotent HSCs and initiates chronic myeloid leukemia (CML).
  • Patients with early phase (also known as chronic phase [CP]) disease usually respond to treatment with ABL tyrosine kinase inhibitors (TKIs), although some patients who respond initially later become resistant.
  • In most patients, TKIs reduce the leukemia cell load substantially, but the cells from which the leukemia cells are derived during CP (so-called leukemia stem cells [LSCs]) are intrinsically insensitive to TKIs and survive long term.
  • LSCs or their progeny can acquire additional genetic and/or epigenetic changes that cause the leukemia to transform from CP to a more advanced phase, which has been subclassified as either accelerated phase or blastic phase disease.
  • Here, we discuss what is known about the molecular mechanisms leading to blastic transformation of CML and propose some novel therapeutic approaches.



64. Deininger M, Schleuning M, Greinix H, Sayer HG, Fischer T, Martinez J, Maziarz R, Olavarria E, Verdonck L, Schaefer K, Boqué C, Faber E, Nagler A, Pogliani E, Russell N, Volin L, Schanz U, Doelken G, Kiehl M, Fauser A, Druker B, Sureda A, Iacobelli S, Brand R, Krahl R, Lange T, Hochhaus A, Gratwohl A, Kolb H, Niederwieser D, European Blood and Marrow Transplantation Group: The effect of prior exposure to imatinib on transplant-related mortality. Haematologica; 2006 Apr;91(4):452-9
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  • BACKGROUND AND OBJECTIVES: Imatinib is an effective treatment for chronic myeloid leukemia (CML) and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL).
  • However, relapse is common in patients with advanced or high risk disease.
  • DESIGN AND METHODS: We retrospectively analyzed 70 patients with CML and 21 with Ph+ ALL who had received imatinib prior to SCT.
  • Multivariate analysis was used to define factors associated with major outcomes (engraftment, graft-versus-host disease, relapse, non-relapse mortality) in addition to descriptive statistics.
  • For the CML patients major outcomes were compared with those of historical controls drawn from the EBMT registry.
  • RESULTS: At SCT, 44% of CML patients were in accelerated phase or blast crisis and 40% of ALL patients had active disease compared to 84% and 95% prior to imatinib.
  • Factors associated with shorter overall and progression-free survival were advanced disease at SCT and a female donor/male recipient pairing.
  • Compared to historical controls, prior imatinib treatment did not influence overall survival, progression-free survival or non-relapse mortality, while there was a trend towards higher relapse mortality and significantly less chronic graft-versus-host disease.
  • [MeSH-minor] Adolescent. Adult. Benzamides. Child. Child, Preschool. Female. Humans. Imatinib Mesylate. Leukemia / mortality. Leukemia / therapy. Male. Middle Aged. Mortality. Retrospective Studies. Treatment Outcome

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  • (PMID = 16585011.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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65. Litzow MR, Dietz AB, Bulur PA, Butler GW, Gastineau DA, Hoering A, Fink SR, Letendre L, Padley DJ, Paternoster SF, Tefferi A, Vuk-Pavlović S: Testing the safety of clinical-grade mature autologous myeloid DC in a phase I clinical immunotherapy trial of CML. Cytotherapy; 2006;8(3):290-8
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  • [Title] Testing the safety of clinical-grade mature autologous myeloid DC in a phase I clinical immunotherapy trial of CML.
  • BACKGROUND: We conducted a phase I clinical immunotherapy trial of CML to evaluate the safety of a clinical-grade leukemic DC product standardized for purity and mature phenotype.
  • METHODS: We injected autologous DC into patients in late chronic or accelerated phases of CML.
  • The patients received mature CD83+ and bcr-abl+ DC prepared from CD14+ cells.
  • T cells drawn later in the course of therapy were more sensitive to stimulation by CML DC in vitro.
  • DISCUSSION: The increase in T-cell sensitivity to CML-specific stimulation that accompanied active immunization by CML DC justifies further clinical studies, possibly with modifications such as an increased frequency and number of DC injections.
  • [MeSH-major] Dendritic Cells / transplantation. Immunotherapy, Active / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy
  • [MeSH-minor] Aged. Antigens, CD / analysis. Antigens, CD14 / analysis. Antigens, CD86 / analysis. Bone Marrow Cells / cytology. Cell Count. Cell Proliferation. Coculture Techniques. Female. Fusion Proteins, bcr-abl / analysis. Humans. Immunoglobulins / analysis. Interferon-gamma / metabolism. Leukocytes, Mononuclear / cytology. Lymphocyte Activation / immunology. Male. Membrane Glycoproteins / analysis. Middle Aged. Myeloid Cells / cytology. Myeloid Cells / immunology. Myeloid Cells / transplantation. T-Lymphocytes / immunology. T-Lymphocytes / metabolism. Transplantation, Autologous. Treatment Outcome

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  • (PMID = 16793737.001).
  • [ISSN] 1465-3249
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 15083; United States / NCI NIH HHS / CA / R01 CA 84368
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD14; 0 / Antigens, CD86; 0 / CD83 antigen; 0 / CD86 protein, human; 0 / Immunoglobulins; 0 / Membrane Glycoproteins; 82115-62-6 / Interferon-gamma; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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66. Voglová J, Maisnar V, Beránek M, Chrobák L: [Combination of imatinib and anagrelide in treatment of chronic myeloid leukemia in blastic phase]. Vnitr Lek; 2006 Sep;52(9):819-22
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  • [Title] [Combination of imatinib and anagrelide in treatment of chronic myeloid leukemia in blastic phase].
  • [Transliterated title] Kombinace imatinibu s anagrelidem v lécbe blastického zvratu chronické myeloidní leukemie.
  • Chronic myeloid leukemia in blast phase (BP) is resistant to chemotherapy and majority of patients die within 6 months.
  • Inhibitor Bcr-Abl tyrosine kinase imatinib mesylate dramatically improved outcome of patients in chronic phase (CP) and is also effective in BP of CML.
  • High platelet counts are often observed at diagnosis or in the subsequent course of the CML in about 25% of patients.
  • Anagrelide selectively reduces circulating platelets and is used in treatment of thrombocythemia in chronic myeloproliferative disorders.
  • Efficacy and safety of combination imatinib mesylate with anagrelide was demonstrated in chronic and accelerated phase of CML.
  • 51-year-old white man with CML presented in blast phase was followed for 4 years.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Blast Crisis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / administration & dosage. Platelet Aggregation Inhibitors / administration & dosage. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Quinazolines / administration & dosage. Thrombocytosis / drug therapy



67. Salerni BL, Bates DJ, Albershardt TC, Lowrey CH, Eastman A: Vinblastine induces acute, cell cycle phase-independent apoptosis in some leukemias and lymphomas and can induce acute apoptosis in others when Mcl-1 is suppressed. Mol Cancer Ther; 2010 Apr;9(4):791-802
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  • [Title] Vinblastine induces acute, cell cycle phase-independent apoptosis in some leukemias and lymphomas and can induce acute apoptosis in others when Mcl-1 is suppressed.
  • Inhibition of the extracellular signal-regulated kinase by PD98059 dramatically accelerates vinblastine-mediated apoptosis in ML-1 leukemia with cells dying in 4 hours from all phases of the cell cycle.
  • Inhibition of protein synthesis by cycloheximide also markedly accelerated vinblastine-induced apoptosis, showing that the proteins required for this acute apoptosis are constitutively expressed.
  • We also investigated the response of 13 other leukemia and lymphoma cell lines and cells from seven chronic lymphocytic leukemia patients.
  • Four cell lines and all chronic lymphocytic leukemia cells were killed in 6 hours by vinblastine alone.

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  • (PMID = 20371726.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009658-17; United States / NCI NIH HHS / CA / CA23108; United States / NCI NIH HHS / CA / CA009658-17; United States / NCI NIH HHS / CA / T32 CA009658; United States / NCI NIH HHS / CA / R01 CA050224; United States / NCI NIH HHS / CA / P30 CA023108-315657; United States / NCI NIH HHS / CA / P30 CA023108; United States / NCI NIH HHS / CA / CA023108-315657; United States / NCI NIH HHS / CA / CA050224-14; United States / NCI NIH HHS / CA / R01 CA050224-14; United States / NCI NIH HHS / CA / CA50224
  • [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 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Flavonoids; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 5V9KLZ54CY / Vinblastine; 98600C0908 / Cycloheximide; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS184304; NLM/ PMC2852489
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68. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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69. Brave M, Goodman V, Kaminskas E, Farrell A, Timmer W, Pope S, Harapanhalli R, Saber H, Morse D, Bullock J, Men A, Noory C, Ramchandani R, Kenna L, Booth B, Gobburu J, Jiang X, Sridhara R, Justice R, Pazdur R: Sprycel for chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia resistant to or intolerant of imatinib mesylate. Clin Cancer Res; 2008 Jan 15;14(2):352-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sprycel for chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia resistant to or intolerant of imatinib mesylate.
  • Food and Drug Administration approved dasatinib (Sprycel; Bristol-Myers Squibb), a new small-molecule inhibitor of multiple tyrosine kinases, for the treatment of adults with chronic phase, accelerated phase, or myeloid or lymphoid blast phase chronic myeloid leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph(+) ALL) with resistance or intolerance to prior therapy including imatinib.
  • The primary efficacy end point in chronic phase CML was major cytogenetic response.
  • The primary end point in accelerated phase, myeloid phase, and lymphoid blast phase CML, and Ph(+) ALL was major hematologic response.
  • In patients with chronic phase CML, the major cytogenetic response rate was 45% with a complete cytogenetic response rate of 33%.
  • Major hematologic response rates in patients with accelerated phase CML, myeloid CML, lymphoid blast CML, and Ph(+) ALL were 59%, 32%, 31%, and 42%, respectively.
  • Median response durations in chronic phase, accelerated phase, and myeloid phase CML had not been reached.
  • The median durations of major hematologic response were 3.7 months in lymphoid blast CML and 4.8 months in Ph(+) ALL.
  • CONCLUSIONS: This report describes the Food and Drug Administration review supporting the approval of dasatinib for CML and Ph(+) ALL based on the rates and durability of cytogenetic and hematologic responses.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Chronic-Phase / drug therapy. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Benzamides. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Dasatinib. Drug Approval. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Multicenter Studies as Topic. Protein Kinase Inhibitors / adverse effects. Protein Kinase Inhibitors / chemistry. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. United States. United States Food and Drug Administration



70. Jabbour E, Cortes J, Kantarjian HM, Giralt S, Jones D, Jones R, Giles F, Andersson BS, Champlin R, de Lima M: Allogeneic stem cell transplantation for patients with chronic myeloid leukemia and acute lymphocytic leukemia after Bcr-Abl kinase mutation-related imatinib failure. Blood; 2006 Aug 15;108(4):1421-3
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  • [Title] Allogeneic stem cell transplantation for patients with chronic myeloid leukemia and acute lymphocytic leukemia after Bcr-Abl kinase mutation-related imatinib failure.
  • Resistance to imatinib mesylate is an emerging problem in the treatment of chronic myeloid leukemia (CML), often associated with point mutations in the Bcr-Abl kinase domain.
  • Ten imatinib-resistant patients with Bcr-Abl kinase mutations received a transplant: 9 had CML (3 in chronic phase, 4 in accelerated phase, and 2 in blast phase) and 1 had Philadelphia-positive acute lymphocytic leukemia (ALL).
  • Disease response was complete molecular (CMR; n = 7), major molecular (n = 2), and no response (n = 1).
  • Allo-SCT remains an important salvage option for patients who develop resistance to imatinib through Bcr-Abl mutations.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Point Mutation. Stem Cell Transplantation
  • [MeSH-minor] Adult. Benzamides. Blast Crisis / genetics. Blast Crisis / metabolism. Blast Crisis / mortality. Blast Crisis / therapy. Disease-Free Survival. Female. Graft Survival / drug effects. Graft Survival / genetics. Humans. Imatinib Mesylate. Male. Middle Aged. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Recurrence. Salvage Therapy. Transplantation, Homologous. Treatment Outcome



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



73. Paydas S, Tanriverdi K, Yavuz S, Seydaoglu G: PRAME mRNA levels in cases with chronic leukemia: Clinical importance and review of the literature. Leuk Res; 2007 Mar;31(3):365-9
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  • [Title] PRAME mRNA levels in cases with chronic leukemia: Clinical importance and review of the literature.
  • The aim of this study is to determine the frequency and the clinical importance of PRAME expression in chronic myeloid leukemia (CML)/chronic myeloproliferative disorders (CMPD) and chronic lymphocytic leukemia (CLL).
  • PRAME mRNA was measured by real time RT-PCR in 88 cases with chronic leukemia (CL) and 42 controls.
  • Seventy cases had CML/CMPD (56 had chronic phase (CP)-14 had accelerated/blastic phase disease (AP/BP) and 18 cases had CLL (11 had early stage (Rai 0-I-II) and 7 had late stage (Rai III-IV).
  • Twenty-four of 70 (34%) cases with CML/CMPD and 5 of 18 (28%) cases with CLL showed PRAME expression.
  • PRAME (+) and PRAME (-) cases were not different for age, Hb, Hct, WBC count, platelet count, stage of the disease and response to therapy.
  • PRAME was monitorised in eight cases during follow-up: in three cases PRAME was negative at CP and expression developed at the AP/BP disease.
  • PRAME was positive at the beginning in five cases (4 CML-1CLL) and expression disappeared after chemotherapy.
  • PRAME mRNA may be a useful marker to detect the minimal residual disease (MRD) and to determine the response to therapy in CLs.
  • [MeSH-major] Antigens, Neoplasm / genetics. Biomarkers, Tumor / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Myeloproliferative Disorders / genetics. RNA, Messenger / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chronic Disease. Disease Progression. Female. Follow-Up Studies. Gene Expression Profiling. Humans. Male. Middle Aged. Neoplasm Staging. Reverse Transcriptase Polymerase Chain Reaction / methods. Treatment Outcome

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  • (PMID = 16914202.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / PRAME protein, human; 0 / RNA, Messenger
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74. 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



75. 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



76. Jabbour E, Kantarjian H, Jones D, Breeden M, Garcia-Manero G, O'Brien S, Ravandi F, Borthakur G, Cortes J: Characteristics and outcomes of patients with chronic myeloid leukemia and T315I mutation following failure of imatinib mesylate therapy. Blood; 2008 Jul 1;112(1):53-5
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  • [Title] Characteristics and outcomes of patients with chronic myeloid leukemia and T315I mutation following failure of imatinib mesylate therapy.
  • Chronic myeloid leukemia (CML) with T315I mutation has been reported to have poor prognosis.
  • At the time of T315I detection, 10 were in chronic phase (CP), 9 in accelerated phase, and 8 in blast phase.
  • Although the T315I mutation is resistant to currently available TKIs, survival of patients with T315I remains mostly dependent on the stage of the disease, with many CP patients having an indolent course.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Point Mutation. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / genetics. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Amino Acid Substitution. Benzamides. Child. Drug Resistance, Neoplasm / genetics. Female. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Male. Middle Aged. Treatment Outcome

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  • (PMID = 18403620.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC4081375
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77. Vidović A, Janković G, Tomin D, Perunicić-Jovanović M, Djunić I, Djurasinović V, Colović M: [Prognostic significance of cellular vascular endothelial growth factor (VEGF) expression in the course of chronic myeloid leukaemia]. Srp Arh Celok Lek; 2009 Jul-Aug;137(7-8):379-83
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  • [Title] [Prognostic significance of cellular vascular endothelial growth factor (VEGF) expression in the course of chronic myeloid leukaemia].
  • INTRODUCTION: Increased angiogenesis in bone marrow is one of the characteristics of chronic myeloid leukaemia (CML), a clonal myeloproliferative disorder that expresses a chimeric bcr/abl protein.
  • The impact of elevated VEGF expression on the course of chronic myeloid leukaemia is unknown.
  • OBJECTIVE: The aim of this study was the follow-up of VEGF expression during the course of CML.
  • METHODS: We studied VEGF expression of 85 CML patients (median age 50 years, range 16-75 years).
  • At the commencement of the study, 29 patients were in chronic phase (CP), 25 in an accelerated phase (AP), and 31 in the blast crisis (BC).
  • The temporal expression (percentage positivity per 1000 analysed cells) VEGF proteins over the course of CML were studied using the immunohistochemical technique utilizing relevant monoclonal antibodies.
  • It was correlated with the laboratory (Hb, WBC and platelet counts, and the percentage of blasts) and clinical parameters (organomegaly, duration of CP, AP, and BC) of disease progression.
  • CONCLUSION: Immunohistochemically confirmed significance of the expression of VEGF in dependence of the CML stage could be of clinical importance in deciding on the timing therapy.
  • These data suggest that VEGF plays a role in the biology of CML and that VEGF inhibitors should be investigated in CML.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 19764591.001).
  • [ISSN] 0370-8179
  • [Journal-full-title] Srpski arhiv za celokupno lekarstvo
  • [ISO-abbreviation] Srp Arh Celok Lek
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Serbia
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A
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78. Li ZJ, Qiu LG, Li X, Mai YJ, Wang GR, Yu Z, Wang YF, Li CH, Li Q: [Expression of beta-Catenin Gene in CML and its relationship with bcr/abl]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Oct;15(5):931-5
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  • [Title] [Expression of beta-Catenin Gene in CML and its relationship with bcr/abl].
  • This study was aimed to quantitatively detect the expression level of beta-catenin and bcr/abl in different phases of chronic myeloid leukemia (CML) and to analyze their potential relationship and significance in the progression of CML.
  • First, the total RNA isolated from BMMNC of patients with CML and donors was reversely transcribed into cDNA.
  • The real-time quantitative PCR method was used to analyze the expression level of beta-catenin and bcr/abl.
  • The expression level of beta-catenin and bcr/abl in different phases of CML was compared and the correlation was analyzed between the two genes.
  • The results showed that the beta-catenin gene in BMMNC of blast crisis of CML patients was expressed significantly higher than that in chronic phase (p < 0.001) and accelerated phase (p = 0.016) of CML patients and in normal donors (p = 0.004).
  • The expression of bcr/abl in blast crisis of CML was statistically higher than that in chronic phase of CML (p = 0.001).
  • The expression levels of beta-catenin and bcr/abl were correlated with each other in CML patients (r = 0.620, p < 0.001).
  • It is concluded that the beta-catenin gene in blast crisis of CML patients express higher than that in chronic phase and accelerated phase of CML, and its expression level is correlated with the level of bcr/abl expression.
  • The increased expression of beta-catenin may be account partly for the blast crisis of CML.

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  • (PMID = 17956664.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / beta Catenin; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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79. Gouda HM, Abdel Mohsen MM: Frequency of expression of RHAMM/CD168 in Egyptian patients with CML. J Egypt Natl Canc Inst; 2009 Jun;21(2):93-9
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  • [Title] Frequency of expression of RHAMM/CD168 in Egyptian patients with CML.
  • It is one of the leukemia-associated antigens (LAA) identified in patients with myeloid leukemias.
  • WE AIMED: at studying the frequency of expression of RHAMM/CD168 in Egyptian patients with CML, both in chronic phase and accelerated/blastic phase, as a potential target structure for cellular immunotherapies, and to compare it with available western records.
  • PATIENTS AND METHODS: RHAMM expression was tested by RT-PCR in peripheral blood mononuclear cells of 60 CML patients divided into 2 groups, group A: 44 chronic phase CML patients, group B: 16 accelerated/ blastic phase patients as well as 15 healthy volunteers.
  • OUR RESULTS: Demonstrated that 14/44 (31.8%) of chronic CML patients showed positive RHAMM expression in contrast to 15/16 ( 93.7%) in the accelerated/blastic phase patients.
  • Moreover within the chronic phase patients the RHAMM positive patients had a significantly higher level of bcr-abl/abl ratio.
  • This highlighted the contribution of RHAMM expression with CML disease progression.
  • CONCLUSION: Our work demonstrated a similar proportion of RHAMM expression in both Egyptian and western CML patients.
  • This may pave the way for subsequent studies suggesting the concomitant use of RHAMM R3 peptide vaccination with conventional CML therapy especially in accelerated phase, in order to achieve complete molecular remission for our patient.
  • [MeSH-major] Antigens, CD44 / genetics. Biomarkers, Tumor / genetics. Cell Proliferation. Extracellular Matrix Proteins / genetics. Leukemia, Myeloid, Chronic-Phase / genetics
  • [MeSH-minor] Adult. Blast Crisis. Case-Control Studies. Female. Fusion Proteins, bcr-abl / genetics. Humans. Male. Middle Aged. Prognosis. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 21057560.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Biomarkers, Tumor; 0 / Extracellular Matrix Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / hyaluronan-mediated motility receptor; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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80. Gucluler G, Baran Y: Docetaxel enhances the cytotoxic effects of imatinib on Philadelphia positive human chronic myeloid leukemia cells. Hematology; 2009 Jun;14(3):139-44
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  • [Title] Docetaxel enhances the cytotoxic effects of imatinib on Philadelphia positive human chronic myeloid leukemia cells.
  • Chronic myelogenous leukemia (CML) results from a translocation between chromosomes 9 and 22 which generates BCR/ABL fusion protein and characterized by uncontrolled proliferation of immature white blood cells.
  • Imatinib, a molecularly targeting anticancer agent, is used widely for the treatment of CML and showed significant activity in chronic and accelerated phases but much less in blast crisis phase.
  • The resistance to imatinib especially in blast crisis phase is recognized as a major problem in the treatment of CML patients.
  • Docetaxel is shown to arrest cells in G2/M phase of the cell cycle which makes cells more sensitive to chemo- and radiotherapy.
  • In this study, we aimed to increase chemosensitivity of human K562 CML cells to imatinib in combination with docetaxel.
  • Taken together, our results showed that the combination of imatinib and docetaxel decreased cellular proliferation and increased apoptosis in human K562 chronic myeloid leukemia cells as compared to any agent alone.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / pharmacology. Pyrimidines / pharmacology. Radiation-Sensitizing Agents / pharmacology. Taxoids / pharmacology

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  • (PMID = 19490758.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Radiation-Sensitizing Agents; 0 / Taxoids; 15H5577CQD / docetaxel; 8A1O1M485B / Imatinib Mesylate; EC 3.4.22.- / Caspase 3
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81. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
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  • (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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82. Imatinib: a second look. Longer follow-up in chronic myeloid leukaemia: clear advantages. Prescrire Int; 2008 Dec;17(98):226-8
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  • [Title] Imatinib: a second look. Longer follow-up in chronic myeloid leukaemia: clear advantages.
  • (1) In 2002/2003, the clinical evaluation of imatinib, a tyrosine kinase inhibitor, in the treatment of chronic myeloid leukaemia left many questions unanswered.
  • (3) As second-line treatment for patients in the chronic phase, we now have non-comparative follow-up data on 532 patients in whom interferon had failed.
  • (4) As second-line treatment for patients in the accelerated phase, we now have non-comparative follow-up data on 235 patients.
  • (9) In practice, imatinib seems to increase survival time when used as a first-line or second-line treatment for patients in different phases of chronic myeloid leukaemia.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 19415889.001).
  • [ISSN] 1167-7422
  • [Journal-full-title] Prescrire international
  • [ISO-abbreviation] Prescrire Int
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines
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83. Shi P, Chandra J, Sun X, Gergely M, Cortes JE, Garcia-Manero G, Arlinghaus RB, Lai R, Amin HM: Inhibition of IGF-IR tyrosine kinase induces apoptosis and cell cycle arrest in imatinib-resistant chronic myeloid leukaemia cells. J Cell Mol Med; 2010 Jun;14(6B):1777-92
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  • [Title] Inhibition of IGF-IR tyrosine kinase induces apoptosis and cell cycle arrest in imatinib-resistant chronic myeloid leukaemia cells.
  • Chronic myeloid leukaemia (CML) is the most common subtype of chronic myeloproliferative diseases.
  • Typically, CML evolves as a chronic phase (CP) disease that progresses into accelerated (AP) and blast phase (BP) stages.
  • In this study, we show that IGF-IR is universally expressed in four CML cell lines.
  • Increased expression levels of IGF-IR with CML progression was supported by quantitative real-time PCR that demonstrated significantly higher levels of IGF-IR mRNA in BP patients.
  • Inhibition of IGF-IR decreased the viability and proliferation of CML cell lines and abrogated their growth in soft agar.
  • Importantly, inhibition of IGF-IR decreased the viability of cells resistant to imatinib mesylate including BaF3 cells transfected with p210 BCR-ABL mutants, CML cell lines and primary neoplastic cells from patients.

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  • (PMID = 19508387.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA114395; United States / NCI NIH HHS / CA / CA114395
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ NIHMS405889; NLM/ PMC3444523
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84. Luo Y, Pan J, Shi JM: [Clinical observation of Gleevec combined with myeloablative allogeneic stem cells transplantation in treatment of chronic myeloid leukemia]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2007 Jul;36(4):343-7
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  • [Title] [Clinical observation of Gleevec combined with myeloablative allogeneic stem cells transplantation in treatment of chronic myeloid leukemia].
  • OBJECTIVE: To observe the efficacy of Gleevec combined with myeloablative allogeneic stem cells transplantation(Allo-SCT) for the treatment of chronic myeloid leukemia (CML).
  • METHODS: Nine patients with CML were treated with Gleevec before and after Allo-SCT, with 5 in the chronic phase (CP), 2 in the accelerated phase (AP) and 2 in the blast-crisis phase (BP).
  • Three cases suffered from acute GVHD and 4 from chronic GVHD.
  • The rate of disease free survival was 88.9% after a median follow-up of 31 m (range 7 approximately 34 m).
  • CONCLUSION: The treatment of CML consisting of myeloablative Allo-SCT combined with Gleevec before and after transplantation is an effective and safe method for CML.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Peripheral Blood Stem Cell Transplantation. Piperazines / therapeutic use. Pyrimidines / therapeutic use



85. Piazza RG, Magistroni V, Franceschino A, Andreoni F, Tornaghi L, Colnaghi F, Corneo G, Pogliani EM, Gambacorti-Passerini C: The achievement of durable complete cytogenetic remission in late chronic and accelerated phase patients with CML treated with Imatinib mesylate predicts for prolonged response at 6 years. Blood Cells Mol Dis; 2006 Sep-Oct;37(2):111-5
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  • [Title] The achievement of durable complete cytogenetic remission in late chronic and accelerated phase patients with CML treated with Imatinib mesylate predicts for prolonged response at 6 years.
  • Despite the positive results achieved by Imatinib mesylate (Imatinib) in the treatment of chronic myeloid leukemia (CML), over the past several years, Imatinib does not eradicate the leukemic clone.
  • Long-term follow-up of CML patients treated with Imatinib will ultimately define the durability of such treatment and the frequency of reemergence of progressive disease.
  • We present the results of a 6-year follow-up of 40 CML patients either in chronic or accelerated phase who obtained a durable (>6 months) complete cytogenetic remission (CCyR) after treatment with Imatinib in a single center.
  • No progressions to more advanced phases of disease have been detected during the follow-up period.
  • Cytogenetic relapse was predicted by either a decrease in the amount of BCR-ABL transcript of less than 2 logs after the achievement of CCyR (p=0.0041) or a time-to-CCyR of more than 12 months (p<0.0001).
  • This 6-year follow-up of the efficacy of Imatinib therapy in CML patients who obtained a durable CCyR indicates that the relapses rate is low over this period of observation and that the rate of relapse does not increase over time.
  • [MeSH-major] Cytogenetic Analysis / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 16908206.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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86. 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



87. Soverini S, Colarossi S, Gnani A, Rosti G, Castagnetti F, Poerio A, Iacobucci I, Amabile M, Abruzzese E, Orlandi E, Radaelli F, Ciccone F, Tiribelli M, di Lorenzo R, Caracciolo C, Izzo B, Pane F, Saglio G, Baccarani M, Martinelli G, GIMEMA Working Party on Chronic Myeloid Leukemia: Contribution of ABL kinase domain mutations to imatinib resistance in different subsets of Philadelphia-positive patients: by the GIMEMA Working Party on Chronic Myeloid Leukemia. Clin Cancer Res; 2006 Dec 15;12(24):7374-9
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  • [Title] Contribution of ABL kinase domain mutations to imatinib resistance in different subsets of Philadelphia-positive patients: by the GIMEMA Working Party on Chronic Myeloid Leukemia.
  • PURPOSE: ABL kinase domain mutations have been implicated in the resistance to the BCR-ABL inhibitor imatinib mesylate of Philadelphia-positive (Ph+) leukemia patients.
  • Mutations were found in 27% of chronic-phase patients (14% treated with imatinib frontline; 31% treated with imatinib post-IFN failure), 52% of accelerated-phase patients, 75% of myeloid blast crisis patients, and 83% of lymphoid blast crisis/Ph+ acute lymphoblastic leukemia (ALL) patients.
  • Mutations were associated in 30% of patients with primary resistance (44% hematologic and 28% cytogenetic) and in 57% of patients with acquired resistance (23% patients who lost cytogenetic response; 55% patients who lost hematologic response; and 87% patients who progressed to accelerated phase/blast crisis).
  • P-loop and T315I mutations were particularly frequent in advanced-phase chronic myeloid leukemia and Ph+ ALL patients, and often accompanied progression from chronic phase to accelerated phase/blast crisis.
  • (c) advanced-phase chronic myeloid leukemia and Ph+ ALL patients have a higher likelihood of developing imatinib-resistant mutations; and (d) the presence of either P-loop or T315I mutations in imatinib-treated patients should warn the clinician to reconsider the therapeutic strategy.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Genes, abl / physiology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Mutation / physiology. Piperazines / therapeutic use. Pyrimidines / therapeutic use



88. 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



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