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1. Jiang Q, Chen SS, Jiang B, Jiang H, Lu Y, Lu DP: [Efficacy and safety evaluation of imatinib in the treatment of patients with chronic granulocytic leukemia in accelerated phase]. Zhonghua Xue Ye Xue Za Zhi; 2004 Jun;25(6):333-6
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  • [Title] [Efficacy and safety evaluation of imatinib in the treatment of patients with chronic granulocytic leukemia in accelerated phase].
  • OBJECTIVE: To evaluate the efficacy and safety of imatinib in the treatment of adult patients with chronic granulocytic leukemia (CGL) in accelerated phase.
  • METHODS: Thirty patients with CGL in accelerated phase were orally administered with imatinib 400 or 600 mg daily for 7 approximately 9 months.
  • RESULTS: Hematological responses occurred in 28 of 30 patients (93.3%) in the treatment: 14 (46.7%) had a complete hematological response, 10 (33.3%) had a marrow response, and 4 (13.3%) returned to chronic phase.
  • Four of these 6 patients had no response and 2 returned to chronic phase again.
  • The risk factors for relapse were blasts > or = 15% in bone marrow or in peripheral blood, extramedullary leukemia involvement, hemoglobin < 100 g/L before the administration of imatinib, and lack of a complete hematological response after the treatment.
  • Cytogenetic remission occurred in 6 of 27 patients (21.4%) after 3 months treatment: 4 (14.3%) were complete cytogenetic response and 2 (7.1%) major cytogenetic response.
  • Mild non-hematologic adverse effects occurred in most of the patients, but were manageable and tolerable, or disappeared automatically.
  • CONCLUSIONS: Imatinib has substantial activity and is well-tolerated in the treatment of accelerated phase of CGL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Aged. Benzamides. Female. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Male. Middle Aged. Treatment Outcome

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  • (PMID = 15308009.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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2. Chen H, Tang L, Peng X, Luo Z, Luo S, Tan W: [Effects of IFN-alpha combined with IL-6 on cell growth and related genes expression and apoptosis of bone marrow cells from CGL patients]. Zhonghua Xue Ye Xue Za Zhi; 2000 Jul;21(7):341-4
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  • [Title] [Effects of IFN-alpha combined with IL-6 on cell growth and related genes expression and apoptosis of bone marrow cells from CGL patients].
  • OBJECTIVE: To investigate the effects of interferon-alpha (IFN-alpha) and IFN-alpha combined with interleukin-6 (IL-6) on cell growth and bcr/abl, bcl-2 and c-myc genes expression in the bone marrow mononuclear cells (MNC) from chronic granulocytic leukemia (CGL) patients.
  • The viable cells were counted and the expression levels of beta-actin, bcr/abl, bcl-2 and c-myc genes were quantitatively detected by reverse transcriptase-polymerase chain reaction (RT-PCR).
  • RESULTS: The cell growth was markedly inhibited by IFN-alpha, but the extent of the inhibition was slightly decreased when IFN-alpha combined with IL-6.
  • The expression levels of bcr/abl and bcl-2 gene were reduced by IFN-alpha or IFN-alpha plus IL-6.
  • The expression of c-myc gene was inhibited by IFN-alpha but promoted by IL-6.
  • CONCLUSIONS: Both IFN-alpha and IFN-alpha plus IL-6 can inhibit the expression of anti-apoptosis genes, and modulate the expression of c-myc.
  • It is the possible mechanism of IFN-alpha therapy for CGL in chronic phase.
  • [MeSH-major] Apoptosis / drug effects. Bone Marrow Cells / drug effects. Interferon-alpha / pharmacology. Interleukin-6 / pharmacology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood
  • [MeSH-minor] Adolescent. Adult. Cell Count. Cell Division / drug effects. Drug Interactions. Fusion Proteins, bcr-abl / genetics. Gene Expression Regulation / drug effects. Humans. Middle Aged. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-myc / genetics. RNA, Messenger / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 11877000.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Interleukin-6; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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3. Lan TY, Lin DT, Tien HF, Yang RS, Chen CY, Wu K: Prognostic factors of treatment outcomes in patients with granulocytic sarcoma. Acta Haematol; 2009;122(4):238-46
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  • [Title] Prognostic factors of treatment outcomes in patients with granulocytic sarcoma.
  • PURPOSE: To investigate the possible prognostic factors of survival outcomes in patients with granulocytic sarcoma (GS).
  • METHODS: We retrospectively investigated the prognostic factors determining survival in 24 patients with GS using Kaplan-Meier survival analysis followed by log rank tests.
  • We evaluated gender, age, location, GS antedating leukemia, underlying disorders, treatment type and stem cell transplantation.
  • RESULTS: The 5-year survival rate for the patients with GS was 21%.
  • The patients undergoing chemotherapy had a significantly longer survival time compared to those who did not (p = 0.0009).
  • We found no difference in the 5-year survival rate among the patients undergoing chemotherapy combined with radiation or surgery.
  • Patients with chronic myelogenous leukemia and myelodysplastic disorders had worse survival rates (p = 0.0028).
  • CONCLUSION: Early diagnosis with biopsy and early chemotherapy can improve survival outcome.
  • [MeSH-major] Sarcoma, Myeloid / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / therapeutic use. Child. Child, Preschool. Combined Modality Therapy. Female. Humans. Kaplan-Meier Estimate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / mortality. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Male. Middle Aged. Myelodysplastic Syndromes / mortality. Myelodysplastic Syndromes / therapy. Prognosis. Retrospective Studies. Translocation, Genetic. Treatment Outcome. Young Adult

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19887783.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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4. Xie XS, Wan DM, Sun H, Sun L, Liu LX, Jiang ZX: [Peripheral blood stem cell transplantation for 53 patients with malignant hematologic diseases]. Ai Zheng; 2007 Apr;26(4):403-6
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  • [Title] [Peripheral blood stem cell transplantation for 53 patients with malignant hematologic diseases].
  • BACKGROUND & OBJECTIVE: Hematopoietic stem cell transplantation could improve the prognosis of malignant hematologic diseases.
  • Peripheral blood stem cell transplantation (PBSCT) has been gradually used as an alternative to bone marrow transplantation (BMT).
  • This study was to observe the efficacy of allogeneic PBSCT (allo-PBSCT) or autologous PBSCT (auto-PBSCT) on malignant hematologic diseases.
  • 2003 to May 2006, 53 patients with malignant hematologic diseases underwent PBSCT in the First Affiliated Hospital of Zhengzhou University.
  • PBSCs were mobilized with granulocyte colony-stimulating factor (G-CSF) or chemotherapy combined with G-CSF.
  • Auto-PBSCT group received infusion of CD34+ cells at a median of 3.0x10(6) cells/kg; allo-PBSCT group received infusion of CD34+ cells at a median of 6.2x106 cells/kg.
  • MAC regimen was used in auto-PBSCT group as conditioning regimen; amended BU/CY regimen was used in allo-PBSCT group.
  • Methotrexate (MTX) combined with cyclosporine A (CsA) and MMF was used for graft-versus-host disease (GVHD) prophylaxis.
  • Antilymphocyte globulin (ALG) was used in 1 patient with 1 mismatched locus in allo-PBSCT group.
  • RESULTS: The median time for neutrophils to reach 0.5x10(9)/L and platelets to reach 20x10(9)/L were 13 days and 19 days in auto-PBSCT group, 12 days and 15 days in allo-PBSCT group.
  • In allo-PBSCT group, grade I-III acute GVHD occurred in 31.4% cases, and chronic GVHD developed in 71.4% cases.
  • The relapse rate was 38.9% in auto-PBSCT group and 5.7% in allo-PBSCT group.
  • The 700-day disease-free survival rate (DFS) was 57.9% in auto-PBSCT group, and 69.5% in allo-PBSCT group.
  • It is a better choice for the cure of malignant hematologic diseases.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Peripheral Blood Stem Cell Transplantation. Transplantation Conditioning
  • [MeSH-minor] Adolescent. Adult. Antigens, CD34 / blood. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Cyclosporine / administration & dosage. Cyclosporine / therapeutic use. Disease-Free Survival. Female. Follow-Up Studies. Graft vs Host Disease / etiology. Graft vs Host Disease / prevention & control. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Male. Methotrexate / administration & dosage. Middle Aged. Mycophenolic Acid / administration & dosage. Mycophenolic Acid / analogs & derivatives. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Transplantation, Homologous. Young Adult

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  • (PMID = 17430661.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD34; 83HN0GTJ6D / Cyclosporine; 9242ECW6R0 / mycophenolate mofetil; HU9DX48N0T / Mycophenolic Acid; YL5FZ2Y5U1 / Methotrexate
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5. Thiele J, Kvasnicka HM, Schmitt-Graeff A, Leder LD, Schaefer HE: Changing patterns of histological subgroups during therapy of Ph1+ chronic myelogenous leukaemia. Histopathology; 2000 Oct;37(4):355-62
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  • [Title] Changing patterns of histological subgroups during therapy of Ph1+ chronic myelogenous leukaemia.
  • AIMS: Bone marrow histopathology reveals a striking heterogeneity at diagnosis of Philadelphia chromosome positive (Ph1+) chronic myelogenous leukaemia (CML).
  • Based on semiquantitative evaluations of the number of megakaryocytes and the content of fibres, various histological subtypes have been postulated.
  • However, little information exists on whether these groups represent stable categories of the different classification systems and whether therapeutic regimes exert any influence on the putative shift of histological patterns.
  • There were at least two representative trephines taken at diagnosis and at median intervals of 16 months.
  • These consisted of a granulocytic (51 patients), a predominantly megakaryocytic (73 patients) and a myelofibrotic pattern (49 patients).
  • Follow-up biopsies revealed that a significant transition of histological groups occurred and that, independently of treatment modalities, the myelofibrotic category was associated with an unfavourable prognosis.
  • Of the 124 patients without myelofibrosis at onset, 42% later transformed into the myelofibrotic subtype.
  • However, these patients showed no prevalence of either a pre-existing granulocytic or megakaryocytic growth.
  • Myelofibrotic changes were significantly associated with interferon (IFN) and busulfan (BU) therapy.
  • On the other hand, a transition of a myelofibrotic into a nonfibrotic subtype was detectable in 17 of the 49 patients under study and related to hydroxyurea (HU) treatment.
  • CONCLUSIONS: Histological classification systems of bone marrow features in CML do not represent stable patterns, but may be significantly altered by therapy, in particular IFN and HU.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Busulfan / therapeutic use. Granulocytes / drug effects. Granulocytes / pathology. Humans. Hydroxyurea / therapeutic use. Interferon-alpha / therapeutic use. Megakaryocytes / drug effects. Megakaryocytes / pathology. Primary Myelofibrosis / drug therapy. Primary Myelofibrosis / pathology. Recombinant Proteins. Retrospective Studies

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  • (PMID = 11012743.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / Recombinant Proteins; 99210-65-8 / interferon alfa-2b; G1LN9045DK / Busulfan; X6Q56QN5QC / Hydroxyurea
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6. Borbolla JR, Nájera A, Arana RM, López-Hernández MA, Mendoza Y, Trueba E: In vivo purging of peripheral blood stem cells obtained by apheresis, using high-dose chemotherapy and granulocyte colony-stimulating factor in chronic myelogenous leukemia patients. J Hematother Stem Cell Res; 2001 Feb;10(1):19-21
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  • [Title] In vivo purging of peripheral blood stem cells obtained by apheresis, using high-dose chemotherapy and granulocyte colony-stimulating factor in chronic myelogenous leukemia patients.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Blood Component Removal. Bone Marrow Purging. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy
  • [MeSH-minor] Adult. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Male. Transplantation, Autologous

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  • (PMID = 11276355.001).
  • [ISSN] 1525-8165
  • [Journal-full-title] Journal of hematotherapy & stem cell research
  • [ISO-abbreviation] J. Hematother. Stem Cell Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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7. Safley AM, Sebastian S, Collins TS, Tirado CA, Stenzel TT, Gong JZ, Goodman BK: Molecular and cytogenetic characterization of a novel translocation t(4;22) involving the breakpoint cluster region and platelet-derived growth factor receptor-alpha genes in a patient with atypical chronic myeloid leukemia. Genes Chromosomes Cancer; 2004 May;40(1):44-50
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  • [Title] Molecular and cytogenetic characterization of a novel translocation t(4;22) involving the breakpoint cluster region and platelet-derived growth factor receptor-alpha genes in a patient with atypical chronic myeloid leukemia.
  • We report a case of BCR-ABL-negative atypical chronic myeloid leukemia (CML) with translocation t(4;22) (q12;q11.2) juxtaposing the breakpoint cluster region (BCR) and platelet-derived growth factor receptor-alpha (PDGFRA) genes.
  • The patient was a 57-year-old man with a history of stage IV diffuse large B-cell lymphoma, status post-6 cycles of combination chemotherapy in 1999, who presented in August 2002 with enlarged lymph nodes, anemia, and marked leukocytosis (50 x 10(9) g/dL) consistent with a myeloproliferative disorder (MPD).
  • A bone marrow biopsy showed granulocytic hyperplasia, neutrophilia, and mild eosinophilia.
  • Initial cytogenetic evaluation by interphase FISH for BCR-ABL, to rule out a translocation 9;22, showed a variant signal pattern consistent with rearrangement of BCR at 22q11.2, but not ABL at 9q34.
  • Analysis of the patient's cDNA by polymerase chain reaction (PCR) for BCR-ABL was negative.
  • PCR amplification and subsequent sequence analysis demonstrated an in-frame 5'-BCR/3'-PDGFRA fusion in the patient's cDNA.
  • PDGFRA encodes a receptor tyrosine kinase and shares structural and organizational homology with the KIT and CSf1R receptor genes.
  • However, although the incidence of MPD involving translocations of PDGFRB has been well established, to our knowledge there are only two previous reports describing a BCR-PDGFRA fusion gene, in 3 patients diagnosed with atypical CML.
  • Here, we report the molecular and cytogenetic characterization of a patient with BCR-PDGFRA-positive MPD who had a complete hematologic response after treatment with imatinib mesylate.
  • [MeSH-major] Chromosome Breakage / genetics. Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 4 / genetics. Cytogenetic Analysis / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Protein-Tyrosine Kinases. Receptor, Platelet-Derived Growth Factor alpha / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Humans. Male. Middle Aged. Myeloproliferative Disorders / genetics. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins c-bcr. Reading Frames / genetics

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  • [Copyright] Copyright 2004 Wiley-Liss, Inc.
  • (PMID = 15034867.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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8. Fang B, Li N, Song Y, Han Q, Zhao RC: Standard-dose imatinib plus low-dose homoharringtonine and granulocyte colony-stimulating factor is an effective induction therapy for patients with chronic myeloid leukemia in myeloid blast crisis who have failed prior single-agent therapy with imatinib. Ann Hematol; 2010 Nov;89(11):1099-105
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  • [Title] Standard-dose imatinib plus low-dose homoharringtonine and granulocyte colony-stimulating factor is an effective induction therapy for patients with chronic myeloid leukemia in myeloid blast crisis who have failed prior single-agent therapy with imatinib.
  • We investigated the efficacy of the induction therapy involving granulocyte colony-stimulating factor (G-CSF) and low-dose homoharringtonine as well as standard-dose imatinib, which we called the G-CSF + homoharringtonine + imatinib (GHI) regimen, in patients with chronic myelogenous leukemia (CML) in blast crisis who have failed prior single-agent therapy with imatinib.
  • The GHI regimen consisted in a unique induction course where imatinib was administered at 400 mg day(-1) until remission, together with homoharringtonine (1 mg/m(2) s.c. twice daily for 14 days every 28 days), and G-CSF, which was administered 1 day before chemotherapy (5 µg/kg s.c. daily).
  • Patients who responded to induction treatment and who had a matched donor received allogeneic hematopoietic stem cell transplantation (allo-HSCT).
  • The results demonstrates that the GHI regimen re-induce hematologic responses or improve the cytogenetic responses in all evaluable patients.
  • Furthermore, eligible patients have benefited from allo-HSCT after response to this induction treatment.
  • We conclude that the GHI regimen may overcome disease-poor response to conventional doses of imatinib and this approach deserves further evaluation as frontline therapy for newly diagnosed CML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blast Crisis / drug therapy. Granulocyte Colony-Stimulating Factor / therapeutic use. Harringtonines / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Benzamides. Drug Therapy, Combination. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Treatment Failure. Treatment Outcome. Young Adult

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  • (PMID = 20499235.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Harringtonines; 0 / Piperazines; 0 / Pyrimidines; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 6FG8041S5B / homoharringtonine; 8A1O1M485B / Imatinib Mesylate
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9. Wisniewski D, Lambek CL, Liu C, Strife A, Veach DR, Nagar B, Young MA, Schindler T, Bornmann WG, Bertino JR, Kuriyan J, Clarkson B: Characterization of potent inhibitors of the Bcr-Abl and the c-kit receptor tyrosine kinases. Cancer Res; 2002 Aug 1;62(15):4244-55
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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 potent inhibitors of the Bcr-Abl and the c-kit receptor tyrosine kinases.
  • The early stage of chronic myelogenous leukemia (CML) is caused by the tyrosine kinase Bcr-Abl.
  • Imatinib mesylate (also known as STI-571 and Gleevec), a tyrosine kinase inhibitor, has shown encouraging results in CML clinical trials and has become a paradigm for targeted cancer therapeutics.
  • Recent reports of resistance to imatinib argue for further development of therapies for CML.
  • During studies of signal transduction, we observed that the pyrido[2,3-d]pyrimidine src tyrosine kinase inhibitor PD173955 inhibited Bcr-Abl-dependent cell growth.
  • Subsequently, a related compound, PD180970, was reported as a potent inhibitor of Bcr-Abl.
  • We have compared the potency of these two compounds and four other analogues with imatinib on Bcr-Abl-dependent cell growth, cytokine-dependent cell growth, and tyrosine kinase inhibition.
  • PD173955 inhibited Bcr-Abl-dependent cell growth with an IC(50) of 2-35 nM in different cell lines.
  • Fluorescence-activated cell-sorting analyses of cells treated with PD173955 showed cell cycle arrest in G(1).
  • PD173955 has an IC(50) of 1-2 nM in kinase inhibition assays of Bcr-Abl, and in cellular growth assays it inhibits Bcr-Abl-dependent substrate tyrosine phosphorylation.
  • Of the six pyrido[2,3-d]pyrimidine analogues studied, PD166326 was the most potent inhibitor of Bcr-Abl-dependent cell growth.
  • PD173955 inhibited kit ligand-dependent c-kit autophosphorylation (IC(50) = approximately 25 nM) and kit ligand-dependent proliferation of M07e cells (IC(50) = 40 nM) but had a lesser effect on interleukin 3-dependent (IC(50) = 250 nM) or granulocyte macrophage colony-stimulating factor (IC(50) = 1 microM)-dependent cell growth.
  • These compounds are potent inhibitors of both the Bcr-Abl and c-kit receptor tyrosine kinases and deserve further study as potential treatments for both CML and for diseases in which c-kit has a role.

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  • (PMID = 12154026.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA064593; United States / NCI NIH HHS / CA / P30 CA008748; United States / NCI NIH HHS / CA / CA08748; United States / NCI NIH HHS / CA / CA64593
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / PD 173955; 0 / PD 180970; 0 / Pyridones; 0 / Pyrimidines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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10. Trumpp A, Essers M, Wilson A: Awakening dormant haematopoietic stem cells. Nat Rev Immunol; 2010 03;10(3):201-9
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  • [Title] Awakening dormant haematopoietic stem cells.
  • Haematopoietic stem cells (HSCs) in mouse bone marrow are located in specialized niches as single cells.
  • During homeostasis, signals from this environment keep some HSCs dormant, which preserves long-term self-renewal potential, while other HSCs actively self renew to maintain haematopoiesis.
  • Interestingly, three factors - granulocyte colony-stimulating factor, interferon-alpha and arsenic trioxide - have been shown to efficiently activate dormant stem cells and thereby could break their resistance to anti-proliferative chemotherapeutics.
  • Thus, we propose that two-step strategies could target resistant leukaemic stem cells by priming tumours with activators of dormancy followed by chemotherapy or targeted therapies.
  • [MeSH-major] Arsenicals / pharmacology. Bone Marrow / immunology. Granulocyte Colony-Stimulating Factor / pharmacology. Hematopoietic Stem Cells / immunology. Interferon-alpha / pharmacology. Oxides / pharmacology
  • [MeSH-minor] Animals. Cell Growth Processes / drug effects. Cell Growth Processes / immunology. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / immunology. Lymphocyte Activation / drug effects. Mice. Stem Cell Niche / immunology

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  • (PMID = 20182459.001).
  • [ISSN] 1474-1741
  • [Journal-full-title] Nature reviews. Immunology
  • [ISO-abbreviation] Nat. Rev. Immunol.
  • [Language] eng
  • [Publication-type] Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Interferon-alpha; 0 / Oxides; 143011-72-7 / Granulocyte Colony-Stimulating Factor; S7V92P67HO / arsenic trioxide
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11. Murohashi I, Yoshida K, Kishimoto K, Takahashi T, Wakao D, Jinnai I, Yagasaki F, Kawai N, Suzuki T, Matsuda A, Hirashima K, Bessho M: Differential response to stem cell factor and Flt3 ligand by the FAB subtype in acute myeloid leukemia clonogenic cells. J Interferon Cytokine Res; 2002 Mar;22(3):335-41
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  • [Title] Differential response to stem cell factor and Flt3 ligand by the FAB subtype in acute myeloid leukemia clonogenic cells.
  • Proliferative response of blast clonogenic cells to various hematopoietic growth factors (HGF), including stem cell factor (SCF) and flt3 ligand (FL) was investigated in 100 patients with acute myeloid leukemia (AML) and chronic myelogenous leukemia (CML) in myeloid crisis (MC).
  • The frequency of spontaneous colony formation was significantly high in CML in MC (55%) and AML French-American-British (FAB) subtype M4 (48%) compared with M2 (16%).
  • The frequency of proliferative response to various HGF alone and in combination according to FAB subtype and CML in MC was as follows: that to granulocyte colony-stimulating factor (G-CSF) was lowest in M1 and CML in MC (50%) compared with other FAB subtypes (>or=86%), that to granulocyte-macrophage CSF (GM-CSF) was lowest in CML in MC (44%) compared with FAB subtypes (>or=74%), and that to interleukin-3 (IL-3) was lowest in CML in MC (30%) compared with FAB subtypes (>or=78%).
  • SCF and FL stimulated blast colony formation in 11% and 17% of patients with M3, respectively, but there was no response to both, and in 60% and 57% of patients with CML in MC, respectively, with 14% showing a response to both.
  • The results are summarized as follows: absence of spontaneous colony formation and response to HGF other than SCF and FL, designated as HGF-dependent growth (M3); spontaneous colony formation and lowest response to HGF, designated as autonomous growth (CML in MC); and spontaneous colony formation and highest response to HGF including SCF and FL, designated as autocrine growth (M4-6).
  • M1 and M2 were intermediate between CML in MC and M4-6.
  • The relation between in vitro growth pattern of blast clonogenic cells and prognosis in AML FAB subtype and CML in MC is discussed.
  • [MeSH-major] Leukemia, Myeloid / drug therapy. Leukemia, Myelomonocytic, Acute / drug therapy. Membrane Proteins / pharmacology. Stem Cell Factor / pharmacology
  • [MeSH-minor] Acute Disease. Blast Crisis / drug therapy. Blast Crisis / pathology. Cell Division / drug effects. Clone Cells. Granulocyte Colony-Stimulating Factor / pharmacology. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. Interleukin-3 / pharmacology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Recombinant Proteins / pharmacology. Retrospective Studies. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 12034041.001).
  • [ISSN] 1079-9907
  • [Journal-full-title] Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
  • [ISO-abbreviation] J. Interferon Cytokine Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-3; 0 / Membrane Proteins; 0 / Recombinant Proteins; 0 / Stem Cell Factor; 0 / Tumor Necrosis Factor-alpha; 0 / flt3 ligand protein; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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12. Bruchová H, Klamová H, Brdicka R: [Gene expression in white blood cells in chronic myeloid leukemia]. Cas Lek Cesk; 2000 Oct 25;139(21):655-9
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  • [Title] [Gene expression in white blood cells in chronic myeloid leukemia].
  • BACKGROUND: The new technologies that have the DNA laboratory over recent years and the general progress in knowledge of the human genome, have allowed the simultaneous observation of the activity of a large number of genes.
  • Chronic myeloid leukemia is characterized with abnormal tyrosine kinase activity of the fused bcr/abl gene, which is most often product of translocation between chromosomes 9 an 22.
  • It is as yet unknown whether this is the only and sufficient cause of the disease, or whether other supporting and co-active abnormalities exist.
  • It is also not yet clear whether an increase of proliferating activity or reduced programmed cell death plays the dominant role.
  • METHODS AND RESULTS: Membrane macroarrays (Clontech 7742-1: Human Cancer cDNA Expression Array with 588 gene probes) were used throughout the study, on which cDNA reverse-transcribed from total RNA in turn isolated from peripheral white blood cells and labelled with 32P was hybridized.
  • Cells obtained from 5 patients with confirmed diagnoses by cytogenetic and molecular (bcr/abl) analyses, but who had not yet been treated by chemotherapy, were the source of the material.
  • In some cases mononuclears and granulocytes were also isolated by Ficoll-Paque centrifugation.
  • Comparison with normal gene expression (healthy donor) was made by subtraction using Clontech AtlaImage 1.5 software.
  • Although changes of expression of identical genes were not observed in all of patients examined, the majority of them were concordant.
  • Values at least double those of the controls applied to the activity of c-jun N-terminal kinase, MMP-8, MMP-9, integrin alpha E, integrin beta and PDGF, whereas the expression of ZAP-70, IRF1, MCL-1, STAT 5B, RARA, CDC25B, RPSA, TNFR decreased.
  • Increases of PCNA, MMP-17, CD59, rho G, CRAF1 and PIG7 or decreases of notch, caspase 8, caspase 4, interleukin 6 receptor, rho B and TIMP1 were observed only in some cell samples.
  • CONCLUSIONS: It seems that some maturation processes and transmembrane signalling are blocked, as well as the effectors of apoptosis.
  • The involvement of both processes-released replication and ineffective apoptosis--was evident; the problem of bcr/abl gene fusion being the necessary first and sufficient step on the way towards developing chronic myeloid leukemia, however, remained unresolved.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Gene Expression Regulation, Leukemic. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukocytes


13. Marley SB, Lewis JL, Schneider H, Rudd CE, Gordon MY: Phosphatidylinositol-3 kinase inhibitors reproduce the selective antiproliferative effects of imatinib on chronic myeloid leukaemia progenitor cells. Br J Haematol; 2004 May;125(4):500-11
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  • [Title] Phosphatidylinositol-3 kinase inhibitors reproduce the selective antiproliferative effects of imatinib on chronic myeloid leukaemia progenitor cells.
  • We investigated the role of the phosphatidylinositol-3 kinase (PI-3K) pathway in regulating the proliferation of primary chronic myeloid leukaemia (CML) progenitor cells by using imatinib to inhibit the activity of p210(Bcr-Abl).
  • The effect of imatinib on the expression of PI-3K pathway proteins was investigated by kinase assays and Western blotting; PI-3K was inhibited by wortmannin or LY294002, Jak2 by AG490 and farnesylation by FTI II; progenitor cell proliferation (self-renewal) was measured by growing myeloid colonies in vitro, then replating them to observe secondary colony formation.
  • Suppression of p210(Bcr-Abl) with imatinib indirectly suppressed the activity of PI-3K and its downstream targets (Erk, Akt and p70S6 kinase), thereby implicating the PI-3K pathway in p210(Bcr-Abl)-mediated signalling in primary CML progenitor cells.
  • The PI-3K inhibitors, wortmannin and LY294002 reproduced the differential effects of imatinib on normal and CML progenitor cell proliferation in vitro by increasing normal cell (P = 0.001) and reducing CML cell proliferation (P = 0.0003).
  • This differential effect was attributable to dysregulated signalling by granulocyte colony-stimulating factor in CML.
  • The responses of individual patient's cells to wortmannin correlated with their responses to imatinib (P = 0.004) but not their responses to AG490 (Jak2 kinase inhibitor) or FTI II (farnesyltransferase inhibitor).
  • Imatinib-resistant K562 cells were sensitive to LY294002.
  • As imatinib-resistant cells remained sensitive to wortmannin and LY294002, targeting the PI-3K pathway may provide an alternative therapy for imatinib-resistant patients.
  • [MeSH-major] Androstadienes / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Piperazines / therapeutic use. Proto-Oncogene Proteins. Pyrimidines / therapeutic use. Signal Transduction / drug effects
  • [MeSH-minor] Alkyl and Aryl Transferases / antagonists & inhibitors. Benzamides. Blotting, Western / methods. Cell Division / drug effects. Cells, Cultured. Chromones / therapeutic use. Drug Therapy, Combination. Farnesyltranstransferase. Humans. Imatinib Mesylate. Interferon-gamma / therapeutic use. Janus Kinase 2. Morpholines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Stem Cells / drug effects. Tyrphostins / therapeutic use


14. Foo J, Drummond MW, Clarkson B, Holyoake T, Michor F: Eradication of chronic myeloid leukemia stem cells: a novel mathematical model predicts no therapeutic benefit of adding G-CSF to imatinib. PLoS Comput Biol; 2009 Sep;5(9):e1000503
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  • [Title] Eradication of chronic myeloid leukemia stem cells: a novel mathematical model predicts no therapeutic benefit of adding G-CSF to imatinib.
  • Imatinib mesylate induces complete cytogenetic responses in patients with chronic myeloid leukemia (CML), yet many patients have detectable BCR-ABL transcripts in peripheral blood even after prolonged therapy.
  • Bone marrow studies have shown that this residual disease resides within the stem cell compartment.
  • Quiescence of leukemic stem cells has been suggested as a mechanism conferring insensitivity to imatinib, and exposure to the Granulocyte-Colony Stimulating Factor (G-CSF), together with imatinib, has led to a significant reduction in leukemic stem cells in vitro.
  • In this paper, we design a novel mathematical model of stem cell quiescence to investigate the treatment response to imatinib and G-CSF.
  • We find that the addition of G-CSF to an imatinib treatment protocol leads to observable effects only if the majority of leukemic stem cells are quiescent; otherwise it does not modulate the leukemic cell burden.
  • The latter scenario is in agreement with clinical findings in a pilot study administering imatinib continuously or intermittently, with or without G-CSF (GIMI trial).
  • Furthermore, our model predicts that the addition of G-CSF leads to a higher risk of resistance since it increases the production of cycling leukemic stem cells.
  • Our results suggest that the additional use of G-CSF may be detrimental to patients in the clinic.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Models, Biological. Neoplastic Stem Cells / drug effects
  • [MeSH-minor] Benzamides. Cell Differentiation / drug effects. Computer Simulation. Drug Synergism. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Imatinib Mesylate. Piperazines / administration & dosage. Pyrimidines / administration & dosage


15. Imamura T, Matsuo S, Yoshihara T, Chiyonobu T, Mori K, Ishida H, Nishimura Y, Kasubuchi Y, Naya M, Morimoto A, Hibi S, Imashuku S: Granulocytic sarcoma presenting with severe adenopathy (cervical lymph nodes, tonsils, and adenoids) in a child with juvenile myelomonocytic leukemia and successful treatment with allogeneic bone marrow transplantation. Int J Hematol; 2004 Aug;80(2):186-9
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  • [Title] Granulocytic sarcoma presenting with severe adenopathy (cervical lymph nodes, tonsils, and adenoids) in a child with juvenile myelomonocytic leukemia and successful treatment with allogeneic bone marrow transplantation.
  • The occurrence of adenopathy in patients with myelodysplastic syndrome-associated extramedullary myeloid cell tumors has rarely been reported.
  • We describe a 7-year-old girl with juvenile myelomonocytic leukemia who showed the novel chromosomal abnormality t(9;12)(p22;q24.1) and who developed severe adenopathy of the cervical lymph nodes, tonsils, and adenoids that was manifested as granulocytic sarcoma.
  • Following chemotherapy, the patient underwent a conditioning regimen of busulfan, cyclophosphamide, and total body irradiation followed by successful allogeneic bone marrow transplantation from her single HLA locus-mismatched mother at 6 months after her diagnosis.
  • The patient continues to be well and in remission 3 years after stem cell transplantation.
  • [MeSH-major] Bone Marrow Transplantation / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Sarcoma, Myeloid / diagnosis. Sarcoma, Myeloid / surgery
  • [MeSH-minor] Adenoids / pathology. Child. Female. Humans. Lymph Nodes / pathology. Palatine Tonsil / pathology. Radiography. Treatment Outcome


16. 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.
  • The present study was designed to investigate whether either continuous or intermittent exposure of these cells to granulocyte-colony stimulating factor (G-CSF) in vitro can overcome this limitation to the effectiveness of imatinib mesylate therapy.
  • 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).
  • Every 4 days, the number of residual undivided viable cells and the total number of viable cells present were measured.
  • RESULTS: Intermittent but not continuous exposure to G-CSF significantly accelerated the disappearance in vitro of initially quiescent CD34(+) CML cells.
  • This resulted in 3- and 5-fold fewer of these cells remaining after 8 and 12 days, respectively, relative to continuous imatinib mesylate alone (P < 0.04).
  • Cultures containing imatinib mesylate and intermittently added G-CSF also showed the greatest reduction in the total number of cells present after 12 days (5-fold more than imatinib mesylate alone).
  • 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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17. Ferrari-Amorotti G, Keeshan K, Zattoni M, Guerzoni C, Iotti G, Cattelani S, Donato NJ, Calabretta B: Leukemogenesis induced by wild-type and STI571-resistant BCR/ABL is potently suppressed by C/EBPalpha. Blood; 2006 Aug 15;108(4):1353-62
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  • [Title] Leukemogenesis induced by wild-type and STI571-resistant BCR/ABL is potently suppressed by C/EBPalpha.
  • Chronic phase-to-blast crisis transition in chronic myelogenous leukemia (CML) is associated with differentiation arrest and down-regulation of C/EBPalpha, a transcription factor essential for granulocyte differentiation.
  • Patients with CML in blast crisis (CML-BC) became rapidly resistant to therapy with the breakpoint cluster region-Abelson murine leukemia (BCR/ABL) kinase inhibitor imatinib (STI571) because of mutations in the kinase domain that interfere with drug binding.
  • We show here that the restoration of C/EBPalpha activity in STI571-sensitive or -resistant 32D-BCR/ABL cells induced granulocyte differentiation, inhibited proliferation in vitro and in mice, and suppressed leukemogenesis.
  • Moreover, activation of C/EBPalpha eradicated leukemia in 4 of 10 and in 6 of 7 mice injected with STI571-sensitive or -resistant 32D-BCR/ABL cells, respectively.
  • Differentiation induction and proliferation inhibition were required for optimal suppression of leukemogenesis, as indicated by the effects of p42 C/EBPalpha, which were more potent than those of K298E C/EBPalpha, a mutant defective in DNA binding and transcription activation that failed to induce granulocyte differentiation.
  • Activation of C/EBPalpha in blast cells from 4 patients with CML-BC, including one resistant to STI571 and BMS-354825 and carrying the T315I Abl kinase domain mutation, also induced granulocyte differentiation.
  • Thus, these data indicate that C/EBPalpha has potent antileukemia effects even in cells resistant to ATP-binding competitive tyrosine kinase inhibitors, and they portend the development of anti-leukemia therapies that rely on C/EBPalpha activation.

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  • (PMID = 16670262.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 95111; United States / PHS HHS / / P01 78890
  • [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 / Benzamides; 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ PMC1895881
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18. Alvarez M: Intracerebral granulocytic sarcoma. J Neurosci Nurs; 2007 Oct;39(5):297-304
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  • [Title] Intracerebral granulocytic sarcoma.
  • Granulocytic sarcomas, also known as chloromas, are rare extramedullary tumors of myeloid or myelocytic origin.
  • They are usually associated with both acute and chronic myelogenous leukemia and myeloproliferative disorders.
  • Leukemia involvement of the central nervous system most commonly presents as meningeal leukemia; intracerebral granulocytic sarcoma (IGS) is rare.
  • Magnetic resonance imaging with and without gadolinium is the imaging of choice to evaluate the tumor; however, tissue biopsy is essential for definitive diagnosis.
  • Treatment usually involves radiation followed by chemotherapy, depending on the previous systemic treatment.
  • Because medical literature about IGS is scarce, optimal treatment is unclear.
  • With the number of leukemia patients in remission, the incidence of IGS is expected to rise.
  • This is because most chemotherapeutic agents do not cross the blood-brain barrier, making the brain a target for leukemia recurrence.
  • Nurses play a vital role in helping patients and families understand the disease process, the treatments involved, and the necessary adjustments, such as performing mundane activities of daily living, especially when neurocognitive impairments are present.
  • [MeSH-major] Brain Neoplasms / diagnosis. Brain Neoplasms / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Sarcoma, Myeloid / diagnosis. Sarcoma, Myeloid / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Biopsy. Blood-Brain Barrier. Cerebral Hemorrhage / etiology. Cognition Disorders / etiology. Headache / etiology. Humans. Incidence. Infection / etiology. Leukemic Infiltration. Magnetic Resonance Imaging. Male. Middle Aged. Nurse's Role / psychology. Patient Education as Topic. Prognosis. Radiotherapy, Adjuvant. Rare Diseases. Tomography, X-Ray Computed. Tumor Lysis Syndrome / etiology

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  • (PMID = 17966297.001).
  • [ISSN] 0888-0395
  • [Journal-full-title] The Journal of neuroscience nursing : journal of the American Association of Neuroscience Nurses
  • [ISO-abbreviation] J Neurosci Nurs
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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19. Ota S, Musashi M, Kondo K, Toyoshima N, Toubai T, Onozawa M, Mori A, Hashino S, Tanaka J, Matsuno K, Imamura M, Asaka M: Effect of imatinib mesylate combined with granulocyte colony-stimulating factor on leukaemic blast cells derived from advanced-stage chronic myelogenous leukaemia patients. Acta Haematol; 2006;116(1):8-18
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  • [Title] Effect of imatinib mesylate combined with granulocyte colony-stimulating factor on leukaemic blast cells derived from advanced-stage chronic myelogenous leukaemia patients.
  • Neutropenia is a severe adverse effect that can occur when treating patients with imatinib mesylate for advanced-stage chronic myelogenous leukaemia (CML).
  • Therefore, we evaluated in vitro the combined effect of imatinib and granulocyte colony-stimulating factor (G-CSF) on proliferation and apoptosis of Bcr-Abl-expressing leukaemic cells to infer the safety of G-CSF administration.
  • In KU812 and K562 cell lines, G-CSF neither stimulated their proliferation nor abolished the suppressive effect of imatinib.
  • However, it stimulated the proliferation of blast cells in 2 out of the 5 cases with advanced-stage CML.
  • These in vitro studies appear to provide data for the decision of G-CSF administration in combination with imatinib in the treatment of neutropenic patients with advanced-stage CML.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cell Proliferation / drug effects. Granulocyte Colony-Stimulating Factor / pharmacology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Piperazines / pharmacology. Pyrimidines / pharmacology
  • [MeSH-minor] Benzamides. Blast Crisis / drug therapy. Blast Crisis / metabolism. Blast Crisis / pathology. Drug Antagonism. Drug Evaluation, Preclinical. Drug Therapy, Combination. Drug-Related Side Effects and Adverse Reactions. Gene Expression Regulation, Leukemic / drug effects. Genes, abl. Humans. Imatinib Mesylate. K562 Cells. Neutropenia / chemically induced. Neutropenia / drug therapy. Neutropenia / metabolism

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  • (PMID = 16809884.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 8A1O1M485B / Imatinib Mesylate
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20. Aschoff P, Häntschel M, Oksüz M, Werner MK, Lichy M, Vogel W, Pfannenberg C: Integrated FDG-PET/CT for detection, therapy monitoring and follow-up of granulocytic sarcoma. Initial results. Nuklearmedizin; 2009;48(5):185-91
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  • [Title] Integrated FDG-PET/CT for detection, therapy monitoring and follow-up of granulocytic sarcoma. Initial results.
  • AIM: Granulocytic sarcomas (GS) are rare extramedullary manifestations of myeloid or lymphoblastic leukaemia.
  • Laboratory examinations are of limited use for diagnosis of extramedullary disease.
  • To date, the possible role of FDG-PET/CT as a method for combined metabolic and morphologic imaging is unclear.
  • We present a series of 10 patients to evaluate the potential role of FDG-PET/CT in the management of GS.
  • The FDG uptake of GS was analyzed and the sensitivity of lesion detection was compared to PET and CT alone.
  • The changes in FDG uptake after therapy were compared to morphological changes detected by CT and follow-up / clinical outcome.
  • RESULTS: 52 untreated or recurrent GS lesions were detected by FDG-PET/CT and all showed an increased FDG uptake with a mean SUVmax and SUVavg of 5.1 and 3.4, respectively.
  • Combined PET/CT avoided 5 false positive findings compared to PET alone and 13 false negative findings and 1 false positive compared to CT alone.
  • Changes in FDG uptake after therapy correlated with clinical outcome and were more reliable than CT assessment alone.
  • Using this metabolic information and morphologic CT criteria, combined FDG-PET/CT was more accurate in lesion detection than FDG-PET or CT alone.
  • Changes in FDG uptake after therapy might be a useful additional parameter for therapy monitoring.
  • [MeSH-major] Sarcoma, Myeloid / radionuclide imaging
  • [MeSH-minor] Adult. Female. Fluorodeoxyglucose F18. Follow-Up Studies. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / radiography. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / radionuclide imaging. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / radiography. Leukemia, Myeloid, Acute / radionuclide imaging. Male. Middle Aged. Neoplasm Staging. Positron-Emission Tomography. Retrospective Studies. Tomography, X-Ray Computed. Young Adult

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  • (PMID = 19710955.001).
  • [ISSN] 0029-5566
  • [Journal-full-title] Nuklearmedizin. Nuclear medicine
  • [ISO-abbreviation] Nuklearmedizin
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
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21. Hashmi KU, Khan B, Ahmed P, Raza S, Hussain I, Mahmood A, Iqbal H, Malik HS, Anwar M: FLAG-IDA in the treatment of refractory/relapsed acute leukaemias: single centre study. J Pak Med Assoc; 2005 Jun;55(6):234-8
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  • [Title] FLAG-IDA in the treatment of refractory/relapsed acute leukaemias: single centre study.
  • OBJECTIVE: To evaluate the efficacy and toxicity profile of the combination of fludarabine, high dose cytarabine, idarubicin, and granulocyte colony stimulating factor in refractory relapsed cases of acute leukaemia, a study is being conducted at Armed Forces Bone Marrow Transplant Centre (AFBMTC) Rawalpindi since January 2003.
  • METHODS: Twelve Patients with refractory/relapsed (Ref/Rel) acute leukaemia (AL) were treated with fludarabine 30 mg/m2 and cytosine arabinoside (AraC) Arac 2 g/m2 for 5 days, idarubicin 10 mg/m2 for 3 days, and granulocyte colony stimulating factor G-CSF 5 micro g/kg from day 0 till neutrophil recovery (ANC > 1.0 x 10(9)/1).
  • Response was evaluated by bone marrow examination on day 20-post chemotherapy.
  • RESULTS: Patients included were refractory acute lymphoblastic leukaemia (ALL) (n=2), relapsed ALL (n = 3), refractory acute myeloid leukaemia (AML) (n = 3), secondary AML (n=2) relapsed AML (n = 1) and acute undifferentiated leukaemia (AUL) (n = 1).
  • Complete remission (CR) was achieved in 8 (66.6%) patients.
  • Three (25%) patients died of post chemotherapy complications and one patient failed to achieve remission.
  • Out of 8 patients who achieved CR, 4 underwent allogeneic bone marrow transfusion (BMT), 1 is being evaluated for the same, 1 received idorubicin, AraC and etopuside (ICE) and high dose AraC, 1 did not receive further chemotherapy and 1 relapsed two months after remission.
  • Seven patients are still in CR after a median follow up of 8 months (range 3-18).
  • CONCLUSION: In our experience, FLAG-IDA is well tolerated and effective regimen in relapsed/refractory acute leukaemias.
  • The toxicity is acceptable, enabling most patients to receive further treatment, including transplantation procedures.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antibiotics, Antineoplastic / therapeutic use. Antimetabolites, Antineoplastic / therapeutic use. Child. Cytarabine / therapeutic use. Female. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Idarubicin / therapeutic use. Male. Middle Aged. Recurrence

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  • (PMID = 16045091.001).
  • [ISSN] 0030-9982
  • [Journal-full-title] JPMA. The Journal of the Pakistan Medical Association
  • [ISO-abbreviation] J Pak Med Assoc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; ZRP63D75JW / Idarubicin
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22. Soliera AR, Lidonnici MR, Ferrari-Amorotti G, Prisco M, Zhang Y, Martinez RV, Donato NJ, Calabretta B: Transcriptional repression of c-Myb and GATA-2 is involved in the biologic effects of C/EBPalpha in p210BCR/ABL-expressing cells. Blood; 2008 Sep 1;112(5):1942-50
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  • [Title] Transcriptional repression of c-Myb and GATA-2 is involved in the biologic effects of C/EBPalpha in p210BCR/ABL-expressing cells.
  • Ectopic C/EBPalpha expression in p210(BCR/ABL)-expressing hematopoietic cells induces granulocytic differentiation, inhibits proliferation, and suppresses leukemogenesis.
  • Upon C/EBPalpha activation, expression of c-Myb and GATA-2 was repressed in 32D-BCR/ABL, K562, and chronic myelogenous leukemia (CML) blast crisis (BC) primary cells but only c-Myb levels decreased slightly in CD34(+) normal progenitors.
  • The role of these 2 genes for the effects of C/EBPalpha was assessed by perturbing their expression in K562 cells.
  • Ectopic c-Myb expression blocked the proliferation inhibition- and differentiation-inducing effects of C/EBPalpha, whereas c-Myb siRNA treatment enhanced C/EBPalpha-mediated proliferation inhibition and induced changes in gene expression indicative of monocytic differentiation.
  • Ectopic GATA-2 expression suppressed the proliferation inhibitory effect of C/EBPalpha but blocked in part the effect on differentiation; GATA-2 siRNA treatment had no effects on C/EBPalpha induction of differentiation but inhibited proliferation of K562 cells, alone or upon C/EBPalpha activation.
  • In summary, the effects of C/EBPalpha in p210(BCR/ABL)-expressing cells depend, in part, on transcriptional repression of c-Myb and GATA-2.
  • Since perturbation of c-Myb and GATA-2 expression has nonidentical consequences for proliferation and differentiation of K562 cells, the effects of C/EBPalpha appear to involve dif-ferent transcription-regulated targets.

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  • (PMID = 18550858.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / PHS HHS / / P01 78890; United States / PHS HHS / / R01 95111
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / DNA Primers; 0 / GATA2 Transcription Factor; 0 / GATA2 protein, human; 0 / RNA, Small Interfering; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC2518896
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23. Petzer AL, Hochenburger E, Haun M, Duba HCh, Grünewald K, Hoflehner E, Sill H, Linkesch W, Gastl G, Gunsilius E: High-dose hydroxyurea plus G-CSF mobilize BCR-ABL-negative progenitor cells (CFC, LTC-IC) into the blood of newly diagnosed CML patients at any time of hematopoietic regeneration. J Hematother Stem Cell Res; 2002 Apr;11(2):293-300
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  • [Title] High-dose hydroxyurea plus G-CSF mobilize BCR-ABL-negative progenitor cells (CFC, LTC-IC) into the blood of newly diagnosed CML patients at any time of hematopoietic regeneration.
  • The objective of this study was to analyze the mobilization kinetics of normal (BCR-ABL(neg)) and malignant (BCR-ABL(pos)) progenitor cells using a new, low toxic, out-patient-based mobilization regimen for Philadelphia chromosome-positive (Ph(pos)) chronic myelogenous leukemia (CML) patients.
  • High doses of hydroxyurea (HD-HU, 3.5 g/m(2) per day, orally for 7 days) followed by granulocyte colony-stimulating factor (G-CSF) (10 microg/kg subcutaneously) were administered to 11 newly diagnosed CML patients.
  • Each apheresis product (n = 30) was individually analyzed for the number and genotype of mature colony-forming cells (CFC) and primitive long-term culture initiating cells (LTC-IC), respectively, by reverse transcription polymerase chain reaction (RT-PCR) of individual colonies.
  • Sufficient numbers of CD34(+) cells/kg bodyweight (BW) could easily be obtained in all patients (median, 15 x 10(6)/kg BW per patient) with a median number of three aphereses performed per patient (range 2-4).
  • Almost each apheresis itself (25/30) contained > or =2 x 10(6) CD34(+) cells/kg BW.
  • All patients with low and intermediate Sokal risk indices (9/11) mobilized primarily BCR-ABL(neg) LTC-IC (median 92%, range 47-100) and CFC (median 89%, range 57-100).
  • Moreover, the mean percentage of BCR-ABL(neg) CFC and LTC-IC in the various apheresis products in these patients did not change throughout the entire time of hematopoietic regeneration.
  • The toxicity of the mobilization procedure was low.
  • Overall, the low toxicity of this regimen, together with the fact that sufficient BCR-ABL(neg) progenitors can be collected throughout the entire period of hematopoietic regeneration, renders this mobilization regimen particularly attractive for the collection of BCR-ABL(neg) progenitors in early chronic phase of Ph(pos) CML.
  • [MeSH-major] Fusion Proteins, bcr-abl / analysis. Granulocyte Colony-Stimulating Factor / administration & dosage. Hematopoietic Stem Cell Mobilization / methods. Hydroxyurea / administration & dosage. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy
  • [MeSH-minor] Adult. Blood Component Removal / standards. Drug Therapy, Combination. Female. Hematopoiesis. Humans. Male. Middle Aged. Pilot Projects. Transplantation, Autologous / methods

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  • (PMID = 11983100.001).
  • [ISSN] 1525-8165
  • [Journal-full-title] Journal of hematotherapy & stem cell research
  • [ISO-abbreviation] J. Hematother. Stem Cell Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor; EC 2.7.10.2 / Fusion Proteins, bcr-abl; X6Q56QN5QC / Hydroxyurea
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24. Liu B, Wang Y, Hao C, Liu Y, Qian L: [Observation of long-term therapeutic outcome in chronic granulocytic leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2001 Feb;22(2):61-3
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  • [Title] [Observation of long-term therapeutic outcome in chronic granulocytic leukemia].
  • OBJECTIVE: To analyse the long-term outcome of various therapeutic protocol for the treatment of chronic granulocytic leukemia (CGL).
  • METHODS: Median duration of chronic phase, survival and transformation of 331 CGL patients treated with different project were retrospectively analyzed.
  • RESULT: Longer chronic phase and survival and lower percentage of transformation were found in patients using mesoindigo as maintaining treatment as compared with those using busulfan as maintaining treatment.
  • These two drugs were both superior to bulsufan.
  • Combination chemotherapy was not superior to meisoindigo, hydroxyurea or busulfan alone.
  • Interferon had the best therapeutic effectiveness for the treatment of CGL.
  • CONCLUSION: Busulfan was not suitable for maintaining treatment.
  • Meisoindigo or meisoindigo combined with hydroxyurea was good choices for maintaining treatment.
  • Interferon could significantly prolong the chronic period and survival period of CGL patients.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Busulfan / therapeutic use. Child. Clinical Trials as Topic. Female. Humans. Male. Middle Aged. Retrospective Studies. Treatment Outcome. Young Adult

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  • (PMID = 11877049.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; G1LN9045DK / Busulfan
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25. Graham SM, Jørgensen HG, Allan E, Pearson C, Alcorn MJ, Richmond L, Holyoake TL: Primitive, quiescent, Philadelphia-positive stem cells from patients with chronic myeloid leukemia are insensitive to STI571 in vitro. Blood; 2002 Jan 1;99(1):319-25
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  • [Title] Primitive, quiescent, Philadelphia-positive stem cells from patients with chronic myeloid leukemia are insensitive to STI571 in vitro.
  • In clinical trials, the tyrosine kinase inhibitor STI571 has proven highly effective in reducing leukemic cell burden in chronic myeloid leukemia (CML).
  • The overall sensitivity of CML CD34(+) progenitor cells to STI571 and the degree to which cell death was dependent on cell cycle status were determined.
  • Stem cells (Lin(-)CD34(+)) from the peripheral blood of patients with CML in chronic phase and from granulocyte-colony-stimulating factor-mobilized healthy donors were labeled with carboxy-fluorescein diacetate succinimidyl diester dye to enable high-resolution tracking of cell division.
  • After culture, the cells were separated by fluorescence-activated cell sorting into populations of viable quiescent versus cycling cells for genotyping.
  • For healthy controls, in the presence of growth factors, STI571 affected neither cell cycle kinetics nor recovery of viable cells.
  • In the absence of growth factors, normal cells were unable to divide.
  • For CML samples, in the presence or absence of growth factors, the response to STI571 was variable.
  • In the most sensitive cases, STI571 killed almost all dividing cells; however, a significant population of viable CD34(+) cells was recovered in the undivided peak and confirmed to be part of the leukemic clone.
  • These studies confirm that CML stem cells remain viable in a quiescent state even in the presence of growth factors and STI571.
  • Despite dramatic short-term responses in vivo, such in vitro insensitivity to STI571, in combination with its demonstrated antiproliferative activity, could translate into disease relapse after prolonged therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Enzyme Inhibitors / pharmacology. Hematopoietic Stem Cells / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / pharmacology. Pyrimidines / pharmacology
  • [MeSH-minor] Antigens, CD34 / analysis. Benzamides. Cell Division / drug effects. Culture Media, Serum-Free. Flow Cytometry. Growth Substances / pharmacology. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Kinetics. Protein-Tyrosine Kinases / antagonists & inhibitors. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured


26. Peng C, Li S: CML mouse model in translational research. Methods Mol Biol; 2010;602:253-66
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  • [Title] CML mouse model in translational research.
  • Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by increased proliferation of granulocytic cells without the loss of their capability to differentiate.
  • CML is derived from the hematopoietic stem cells (1) with the Philadelphia chromosome resulting from of a reciprocal translocation between the chromosomes 9 and 22 t(9;22)-(q34;q11).
  • This translocation produces a fusion gene known as BCR-ABL which acquires uncontrolled tyrosine kinase activity, constantly turning on its downstream signaling molecules/pathways, and promoting proliferation of leukemia cell through anti-apoptosis and acquisition of additional mutations.
  • To evaluate the role of each critical downstream signaling molecule of BCR-ABL and test therapeutic drugs in vivo, it is important to use physiological mouse disease models.
  • In this chapter, we describe a mouse model of CML induced by BCR-ABL retrovirus (MSCV-BCR-ABL-GFP; MIG-BCR-ABL) and how to use this model in translational research.
  • [MeSH-major] Disease Models, Animal. Fusion Proteins, bcr-abl. Signal Transduction / physiology. Translational Medical Research / methods
  • [MeSH-minor] Animals. Antineoplastic Agents / metabolism. Antineoplastic Agents / therapeutic use. Benzamides. Bone Marrow Cells / cytology. Cell Line. Cell Transplantation / methods. HSP90 Heat-Shock Proteins / antagonists & inhibitors. HSP90 Heat-Shock Proteins / metabolism. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Piperazines / metabolism. Piperazines / therapeutic use. Protein Kinase Inhibitors / metabolism. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / metabolism. Pyrimidines / therapeutic use. Transduction, Genetic

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  • (PMID = 20012403.001).
  • [ISSN] 1940-6029
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / HSP90 Heat-Shock Proteins; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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27. Zheng C, Pisa P, Stromberg O, Blennow E, Hansson M: Generation of dendritic cells from peripheral blood of patients at different stages of chronic myeloid leukemia. Med Oncol; 2000 Nov;17(4):270-8
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  • [Title] Generation of dendritic cells from peripheral blood of patients at different stages of chronic myeloid leukemia.
  • We report a method to generate dendritic cells (DC) from frozen leukapheresis products of patients with chronic myeloid leukemia (CML), using sterile culture bags and serum-free culture medium, ie conditions feasible for re-infusion into the patient as part of immunotherapeutic protocols.
  • Leukapheresis products were stored from harvests performed either at diagnosis (13 patients) or after chemotherapy with subsequent granulocyte colony stimulating factor (G-CSF) administration (9 patients), for Peripheral Blood Stem Cell (PBSC) collections.
  • In the presence of optimal concentrations of GM-CSF (50 ng/ml) and IL-4 (40 ng/ml) CML progenitors differentiated on day 7 and 14 of culture to DC, expressing CD1a,HLA-DR and CD86 surface antigens.
  • Mature DCs exhibited on average 12-fold higher allo-stimulatory capacity for CD4+ and CD8+ cells compared to non-cultured PBMC in mixed lymphocyte reaction (MLR).
  • Only DCs obtained from CML patients at diagnosis exhibited bcr/abl fusion gene when tested by fluorescent in situ hybridization (FISH).
  • CD34-selection on leukapheresis products from diagnosis (7 patients) resulted in later maturation of DCs (after 14-15 d), compared to the nonselected PBMC.
  • Large differences were observed between individual patients and different leukapheresis products from the same patient.
  • Our report demonstrates the possibility to generate ex vivo autologous functionally active DC in CML in a way that allows their clinical application as immunotherapeutic agents.
  • [MeSH-major] Dendritic Cells. Leukapheresis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • [MeSH-minor] Antigens, CD34. Cell Culture Techniques / methods. Cell Survival. Cryopreservation. Culture Media. Granulocyte-Macrophage Colony-Stimulating Factor / administration & dosage. Humans. Immunotherapy / methods. Interleukin-4 / administration & dosage. Tumor Cells, Cultured

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  • (PMID = 11114705.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Culture Media; 207137-56-2 / Interleukin-4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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28. Saydam G, Aydin HH, Sahin F, Selvi N, Oktem G, Terzioglu E, Buyukkececi F, Omay SB: Involvement of protein phosphatase 2A in interferon-alpha-2b-induced apoptosis in K562 human chronic myelogenous leukaemia cells. Leuk Res; 2003 Aug;27(8):709-17
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  • [Title] Involvement of protein phosphatase 2A in interferon-alpha-2b-induced apoptosis in K562 human chronic myelogenous leukaemia cells.
  • Interferon-alpha (IFN-alpha)-2b is known to have antiproliferative effects on hematological malignant cells, especially chronic myelogenous leukaemia (CML).
  • However, it can induce cytogenetical remissions in a very small percentage of the patients.
  • Also during interferon therapy, resistance can emerge in the CML clones.
  • K562 is an in vitro model cell line transformed from a Ph positive CML patient.
  • It can be induced to differentiate to granulocytic and/or monocytic lineages with certain molecules.
  • IFN-alpha-2b generally exerts its effects on CML cells by Janus family kinases (Jak/Stat) pathway, mostly through tyrosine kinase system.
  • However, there is almost no data on the relevance of serine/threonine (Ser/Thr) protein phosphatase (PP) system in the interferon induced signal transduction pathways.
  • In this study, we investigated serine/threonine protein phosphatases in the IFN-alpha-2b induced K562 cytotoxicity.
  • Trypan blue dye exclusion test and MTT assay were utilised for determining cytotoxicity.
  • IC(50) of IFN-alpha-2b on K562 cells was found to be 600IU/ml.
  • However, no differentiation was determined by analysis of cell surface antigen expressions.
  • Serine/threonine protein phosphatase inhibitors calyculin A (Cal A) and okadaic acid (OKA) augmented the IFN-alpha-2b induced cytotoxicity.
  • Apoptosis assay by the mono-oligonucleosome detection and acridine orange/propidium iodide dye revealed marked apoptosis underlying cytotoxicity.
  • Phosphatase enzyme assay revealed a gradual increase in protein phosphatase 2A (PP2A) activity during interferon induced cytotoxicity.
  • In conclusion, PP2A plays a role in IFN-alpha-2b induced apoptosis of K562 cells and should be investigated as a new window furthermore.
  • [MeSH-major] Apoptosis / drug effects. Interferon-alpha / pharmacology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Phosphoprotein Phosphatases / physiology
  • [MeSH-minor] Cell Differentiation / drug effects. Enzyme Inhibitors / pharmacology. Humans. Inhibitory Concentration 50. K562 Cells. Kinetics. Protein Phosphatase 2. Protein Subunits / analysis. Recombinant Proteins

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  • (PMID = 12801529.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Interferon-alpha; 0 / Protein Subunits; 0 / Recombinant Proteins; 99210-65-8 / interferon alfa-2b; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / Protein Phosphatase 2
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29. Smith BD, Kasamon YL, Kowalski J, Gocke C, Murphy K, Miller CB, Garrett-Mayer E, Tsai HL, Qin L, Chia C, Biedrzycki B, Harding TC, Tu GH, Jones R, Hege K, Levitsky HI: K562/GM-CSF immunotherapy reduces tumor burden in chronic myeloid leukemia patients with residual disease on imatinib mesylate. Clin Cancer Res; 2010 Jan 1;16(1):338-47
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  • [Title] K562/GM-CSF immunotherapy reduces tumor burden in chronic myeloid leukemia patients with residual disease on imatinib mesylate.
  • PURPOSE: Chronic myeloid leukemia (CML) can be responsive to T-cell-mediated immunity.
  • K562/granulocyte macrophage-colony stimulating factor (GM-CSF) is a GM-CSF producing vaccine derived from a CML cell line that expresses several CML-associated antigens.
  • A pilot study was developed to determine if K562/GM-CSF immunotherapy could improve clinical responses to imatinib mesylate (IM) in patients with chronic myeloid leukemia.
  • EXPERIMENTAL DESIGN: Patients with chronic phase CML who achieved at least a major cytogeneic response but remained with persistent, measurable disease despite one or more years on imatinib mesylate were eligible.
  • CML disease burden was measured serially before and after vaccination.
  • RESULTS: Nineteen patients were vaccinated, with a median duration of previous imatinib mesylate therapy of 37 (13-53) months.
  • Mean PCR measurements of BCR-ABL for the group declined significantly following the vaccines (P = 0.03).
  • Thirteen patients had a progressive decline in disease burden, 8 of whom had increasing disease burden before vaccination.
  • CONCLUSIONS: K562/GM-CSF vaccine appears to improve molecular responses in patients on imatinib mesylate, including achieving complete molecular remissions, despite long durations of previous imatinib mesylate therapy.

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  • (PMID = 20048335.001).
  • [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 States / NCI NIH HHS / CA / CA108174-01; United States / NCI NIH HHS / CA / R21 CA108174; United States / NCI NIH HHS / CA / 1R21CA108174-01; United States / NCI NIH HHS / CA / R21 CA108174-01
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Benzamides; 0 / Cancer Vaccines; 0 / Piperazines; 0 / Pyrimidines; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; 8A1O1M485B / Imatinib Mesylate; 99011-02-6 / imiquimod; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ NIHMS159836; NLM/ PMC2804932
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30. Ghalaut VS, Pahwa MB, Sunita, Ghalaut PS: Alteration in lipid profile in patients of chronic myeloid leukemia before and after chemotherapy. Clin Chim Acta; 2006 Apr;366(1-2):239-42
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  • [Title] Alteration in lipid profile in patients of chronic myeloid leukemia before and after chemotherapy.
  • BACKGROUND: Chronic myeloid leukemia (CML) is a myeloproliferative disorder of pleuripotent hematopoietic progenitor cells characterized by excessive proliferation and accumulation of granulocytes and occasionally red blood cells and platelets.
  • METHODS: We examined 30 newly diagnosed and proved cases of CML admitted in medical wards or attending a clinical hematology clinic.
  • In addition to routine hematological investigations, lipid profile was done in all the patients at the time of presentation, 4-6 weeks after the start of chemotherapy and 6 months after the chemotherapy even if some of the patients were not in remission.
  • RESULTS: Total serum cholesterol, HDL-cholesterol and LDL-cholesterol concentrations increased significantly after chemotherapy whereas serum triglyceride and VLDL-C cholesterol concentrations did not increase significantly.
  • Also, lipid concentrations were correlated with disease activity.
  • Serum triglyceride and VLDL-C concentrations were inversely related to the hemoglobin concentrations.
  • We found from the present study that low lipid concentrations are associated with poor prognosis of the disease.
  • CONCLUSION: We suggest that the estimation of lipid profile may be helpful in evaluating the response to chemotherapy in CML patients.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood. Lipids / blood
  • [MeSH-minor] Adolescent. Adult. Aged. Cholesterol / blood. Cholesterol, HDL / blood. Cholesterol, LDL / blood. Cholesterol, VLDL / blood. Female. Humans. Male. Middle Aged. Remission Induction. Time Factors. Treatment Outcome. Triglycerides / blood

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  • (PMID = 16386722.001).
  • [ISSN] 0009-8981
  • [Journal-full-title] Clinica chimica acta; international journal of clinical chemistry
  • [ISO-abbreviation] Clin. Chim. Acta
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cholesterol, HDL; 0 / Cholesterol, LDL; 0 / Cholesterol, VLDL; 0 / Lipids; 0 / Triglycerides; 97C5T2UQ7J / Cholesterol
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31. Kantarjian HM, O'Brien S, Cortes J, Giles FJ, Faderl S, Issa JP, Garcia-Manero G, Rios MB, Shan J, Andreeff M, Keating M, Talpaz M: Results of decitabine (5-aza-2'deoxycytidine) therapy in 130 patients with chronic myelogenous leukemia. Cancer; 2003 Aug 1;98(3):522-8
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  • [Title] Results of decitabine (5-aza-2'deoxycytidine) therapy in 130 patients with chronic myelogenous leukemia.
  • BACKGROUND: General and site-specific DNA methylation is associated with tumor progression and resistance in several cancers, including chronic myelogenous leukemia (CML).
  • Decitabine is a hypomethylating agent that has shown encouraging preliminary anti-CML activity.
  • This study evaluated the activity and toxicity of decitabine in different phases of CML.
  • METHODS: One hundred and thirty patients with CML were treated: 123 with Philadelphia chromosome (Ph)-positive CML (64 blastic, 51 accelerated, 8 chronic) and 7 with Ph-negative CML.
  • Only four patients (3%) died during the first course from myelosuppressive complications (three patients) or progressive disease (one patient).
  • Of 64 patients in the CML blastic phase, 18 patients (28%) achieved objective responses.
  • Of these 18 patients, 6 achieved complete hematologic responses (CHR), 2 achieved partial hematologic responses (PHR), 7 achieved hematologic improvements (HI), and 3 returned to the second chronic phase (second CP).
  • Among eight patients treated in the chronic phase, five (63%) had objective responses.
  • Of seven patients treated for Ph-negative CML, four (57%) had objective responses.
  • There was no evidence of a dose-response effect.
  • The estimated 3-year survival rate was less than 5% in the blastic phase and 27% in the accelerated phase.
  • With decitabine 50-75 mg/m(2), the median time to granulocyte recovery above 0.5 x 10(9)/L was about 4 weeks.
  • CONCLUSIONS: Decitabine appears to have significant anti-CML activity.
  • Future studies should evaluate lower-dose, longer-exposure decitabine schedules alone in imatinib-resistant CML, as well as combinations of decitabine and imatinib in different CML phases.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / analogs & derivatives. Azacitidine / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Blast Crisis. DNA Modification Methylases / antagonists & inhibitors. Drug Administration Schedule. Female. Humans. Male. Middle Aged

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  • [Copyright] Copyright 2003 American Cancer Society.DOI 10.1002/cncr.11543
  • (PMID = 12879469.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
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32. Ulrich CM, Yasui Y, Storb R, Schubert MM, Wagner JL, Bigler J, Ariail KS, Keener CL, Li S, Liu H, Farin FM, Potter JD: Pharmacogenetics of methotrexate: toxicity among marrow transplantation patients varies with the methylenetetrahydrofolate reductase C677T polymorphism. Blood; 2001 Jul 1;98(1):231-4
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  • This study investigated whether a polymorphism in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene (C677T) modifies responses to methotrexate (MTX) in patients undergoing bone marrow transplantation.
  • About 10% to 12% of the population carry the MTHFR TT genotype (enzyme activity, 30% of wild type [CC]).
  • Patients (n = 220) with chronic myelogenous leukemia underwent marrow allografts and were given a short course of MTX.
  • MTX toxicity measures included the oral mucositis index (OMI), speed of engraftment (platelet and granulocyte counts), and bilirubin.
  • Platelet counts recovered more slowly among patients with the TT genotype compared to wild type (24% slower recovery to 10 000 platelets/microL, P =.23; 34% slower to 20 000/microL, P =.08).
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Methotrexate / pharmacokinetics. Oxidoreductases Acting on CH-NH Group Donors / genetics
  • [MeSH-minor] Adult. Bilirubin / blood. Biotransformation. Cohort Studies. Female. Genotype. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukocyte Count. Male. Methylenetetrahydrofolate Reductase (NADPH2). Middle Aged. Mouth Mucosa. Platelet Count. Point Mutation. Polymorphism, Genetic. Stomatitis / chemically induced. Stomatitis / etiology. Stomatitis / genetics

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  • [CommentIn] Blood. 2001 Oct 1;98(7):2283-4 [11592264.001]
  • (PMID = 11418485.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA15704; United States / NCI NIH HHS / CA / CA18029; United States / NCI NIH HHS / CA / CA18221; United States / NIEHS NIH HHS / ES / ES-07033; United States / NHLBI NIH HHS / HL / HL36444
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.5.- / Oxidoreductases Acting on CH-NH Group Donors; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2); RFM9X3LJ49 / Bilirubin; YL5FZ2Y5U1 / Methotrexate
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33. Moen MD, McKeage K, Plosker GL, Siddiqui MA: Imatinib: a review of its use in chronic myeloid leukaemia. Drugs; 2007;67(2):299-320
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  • [Title] Imatinib: a review of its use in chronic myeloid leukaemia.
  • Imatinib (Gleevec, Glivec) is a synthetic tyrosine kinase inhibitor used in the treatment of chronic myeloid leukaemia (CML).
  • It is specifically designed to inhibit the breakpoint cluster region (BCR)-Abelson (ABL) fusion protein that results from the chromosomal abnormality known as the Philadelphia chromosome.
  • CML is characterised by this abnormality, which leads to abnormalities of the peripheral blood and bone marrow including an increase in the number of granular leukocytes.
  • Imatinib is approved in numerous countries worldwide for the treatment of newly diagnosed Philadelphia chromosome-positive (Ph+) chronic-phase CML, Ph+ accelerated-phase or blast-crisis CML, and in patients with Ph+ chronic-phase CML who have failed to respond to interferon-alpha therapy.
  • It is also indicated in paediatric patients with newly diagnosed Ph+ chronic-phase CML, in accelerated-phase or blast-crisis CML, or in chronic-phase CML after failure of interferon-alpha therapy or when the disease has recurred after haematopoietic stem cell transplantation (HSCT).
  • Imatinib is effective and generally well tolerated in patients with Ph+ CML.
  • In patients with newly diagnosed chronic-phase CML, imatinib was more effective than interferon-alpha plus cytarabine in preventing progression of the disease and in achieving haematological and cytogenetic responses.
  • Overall survival rates remain high after 5 years of follow-up, and historical comparisons with other treatments demonstrate improved overall survival with imatinib in the long term.
  • Patients with accelerated-phase or blast-crisis CML, or those who have not responded to prior interferon-alpha therapy also benefit from imatinib treatment.
  • Some patients become resistant or intolerant to imatinib therapy; management strategies to overcome these problems include dosage adjustment, other treatments, or combination therapy with imatinib and other agents.
  • Allogeneic HSCT is currently the only potentially curative treatment, but it is associated with high rates of morbidity and mortality and is not suitable for all patients.
  • The introduction of imatinib has had a marked impact on outcomes in patients with CML.
  • It remains a valuable treatment for all stages of the disease, especially initial treatment of newly diagnosed Ph+ chronic-phase CML, and is endorsed by European and US treatment guidelines as a first-line option.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Cost-Benefit Analysis. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate

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  • (PMID = 17284091.001).
  • [ISSN] 0012-6667
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 90
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34. Robak T: Purine nucleoside analogues in the treatment of myleoid leukemias. Leuk Lymphoma; 2003 Mar;44(3):391-409
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  • [Title] Purine nucleoside analogues in the treatment of myleoid leukemias.
  • The purine nucleoside analogues (PNA), fludarabine (FA), cladribine (2-chlorodeoxyadenosine, 2-CdA) and 2'-deoxycoformycin (DCF), represent a novel group of cytotoxic agents with high activity in low-grade lymphoid malignancies.
  • However, several investigations have revealed that these agents are active also in acute myeloid leukemia (AML) and chronic myelogenous leukemia (CML).
  • Synergistic interaction between FA or 2-CdA with cytarabine (Ara-C) have been demonstrated in both preclinical and clinical studies.
  • PNA enhance the cell concentration of Ara-CTP, which is active metabolite of Ara-C.
  • It is likely that the addition of granulocyte colony stimulating factor (G-CSF) may further improve the effects of FA (FLAG) or 2-CdA (CLAG).
  • The addition of anthracyclines to induction therapy does not appear to result in a substantial advantage in terms of CR achievement and duration.
  • An alternative approach to increase FLAG activity might be the addition of investigational drugs with novel mechanism of action, such as topoiromerase I inhibitors.
  • The addition of anthracyclines to induction therapy does not appear to result in a substantial advantage in terms of CR achievement and duration.
  • Clinical studies have confirmed the efficacy of PNA alone or in combination protocols in the treatment of AML.
  • These regimens seem to produce superior results with acceptable toxicities in previously treated and relapsed, poor risk AML.
  • However, early relapses remain a significant problem in a majority of refractory or relapsed patients in CR after treatment with PNA based regimens.
  • To prolong remission duration or even cure AML, auto--or allo stem cell transplantation should be considered.
  • However, FAMP or 2-CdA containing regimens may impair mobilization and collection of stem cells from peripheral blood for autotransplantation.
  • Few studies have analyzed the role of PNA in CML.
  • 2-CdA, FAMP and DCF can induce hematologic response in chronic phase of CML but cytogenetic responses have not been observed.
  • Preliminary results suggest, that PNA used alone or in combination may be used as palliation in blast phase of the disease.
  • However, currently, the role of these agents in CML is insignificant because of the high activity of Glivec in this disease.
  • Finally, PNA, especially FA play an important role in non-myeloablative conditioning regimens for allogenic stem cell transplantation in high-risk patients, possibly also with myeloid malignancies.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Cladribine / therapeutic use. Leukemia, Myeloid / drug therapy. Pentostatin / therapeutic use. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antibiotics, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Clinical Trials as Topic. Cytarabine / administration & dosage. Drug Synergism. Female. Granulocyte Colony-Stimulating Factor / administration & dosage. Hematopoietic Stem Cell Mobilization. Humans. Infant. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Male. Middle Aged. Peripheral Blood Stem Cell Transplantation. Remission Induction. Salvage Therapy. Transplantation Conditioning. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 12688309.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 395575MZO7 / Pentostatin; 47M74X9YT5 / Cladribine; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; FLAG protocol
  • [Number-of-references] 128
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35. Morita R, Hashino S, Sogabe S, Dazai M, Onozawa M, Izumiyama K, Kondo T, Ota S, Kobayashi S, Imamura M, Asaka M: [Imatinib mesylate plus G-CSF therapy for chronic myelogenous leukemia in the blastic crisis]. Rinsho Ketsueki; 2004 Oct;45(10):1105-10
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  • [Title] [Imatinib mesylate plus G-CSF therapy for chronic myelogenous leukemia in the blastic crisis].
  • Imatinib mesylate (imatinib) has shown significant effects in patients with chronic myelogenous leukemia.
  • However, hematological toxicity often occurs and requires dosage reduction or discontinuation of imatinib treatment.
  • A patient with chronic myelogenous leukemia in the blastic crisis received granulocyte-colony stimulating factor (G-CSF) simultaneously with imatinib.
  • There are a few reports on the efficacy of combined therapy with G-CSF and imatinib; however, the results in our case are rare suggesting that the use of G-CSF is effective for preventing severe infection.
  • G-CSF enables continuous treatment with high-dose imatinib.
  • [MeSH-major] Blast Crisis / drug therapy. Granulocyte Colony-Stimulating Factor / administration & dosage. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Bacterial Infections / prevention & control. Benzamides. Drug Therapy, Combination. Fatal Outcome. Humans. Imatinib Mesylate. Male. Middle Aged. Neutropenia / prevention & control. Remission Induction

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  • (PMID = 15553045.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 8A1O1M485B / Imatinib Mesylate
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36. Gómez-Almaguer D, Ruiz-Argüelles GJ, González-Llano O, Ruiz-Argüelles A, Cantú-Rodríguez OG: [Peripheral blood hematopoietic cell transplant using immunosuppressive chemotherapy without bone marrow destruction: "minitransplant"]. Gac Med Mex; 2002 May-Jun;138(3):235-9
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  • [Title] [Peripheral blood hematopoietic cell transplant using immunosuppressive chemotherapy without bone marrow destruction: "minitransplant"].
  • [Transliterated title] Trasplante de células hematopoyéticas de sangre periférica utilizando quimioterapia inmunosupresora sin destrucción de la médula ósea: "minitrasplante".
  • Using a nonmyeloablative, immunosuppressive, fludarabine (FLU)-base conditioning regimen, we have performed allogeneic peripheral blood stem cell transplants in 17 patients (six with chronic granulocytic leukemia, four with acute myelogenous leukemia, five with acute lymphoblastic leukemia, one with myelodysplasia and one, with thalassemia major).
  • Conditioning regimen consisted of FLU/busulfan/cyclophosphamide or FLU melphalan.
  • To avoid graft vs. host disease (GVHD), cyclosporine and methotrexate were used.
  • Median granulocyte recovery time to 0.5 x 10(9) was 11 days, whereas median platelet recovery time to 20 x 10(9) was 12 days.
  • Seven patients did not need red blood cell transfusions and four did not need platelet transfusions.
  • In thirteen individuals (76%), the procedure could be completed fully on an outpatient basis.
  • Follow-up times range between 1 and 14 months.
  • Five of 17 patients developed acute GVHD whereas 4/10 developed chronic GVHD.
  • Five patients (29%) have died, three due to relapse of the disease and two due to GVHD.
  • This procedure is substantially less costly than its counterpart, using in-hospital myeloablative conditioning regimens, and may represent another approach in management of patients requiring allogeneic stem cell transplant.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / therapeutic use. Busulfan / administration & dosage. Busulfan / therapeutic use. Child. Child, Preschool. Cyclophosphamide / administration & dosage. Cyclophosphamide / therapeutic use. Cyclosporins / administration & dosage. Cyclosporins / therapeutic use. Female. Follow-Up Studies. Graft vs Host Disease / prevention & control. Humans. Immunosuppressive Agents / administration & dosage. Immunosuppressive Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / therapy. Male. Melphalan / administration & dosage. Melphalan / therapeutic use. Methotrexate / administration & dosage. Methotrexate / therapeutic use. Middle Aged. Neural Tube Defects / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Time Factors. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use

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  • (PMID = 12096391.001).
  • [ISSN] 0016-3813
  • [Journal-full-title] Gaceta médica de México
  • [ISO-abbreviation] Gac Med Mex
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Cyclosporins; 0 / Immunosuppressive Agents; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan; YL5FZ2Y5U1 / Methotrexate
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37. Ruiz-Argüelles GJ: [Graft vs. tumor effect in chronic granulocytic leukemia]. Rev Invest Clin; 2002 Mar-Apr;54(2):154-60
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  • [Title] [Graft vs. tumor effect in chronic granulocytic leukemia].
  • [Transliterated title] El efecto de injerto contra tumor en leucemia granulocítica crónica.
  • [MeSH-major] Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Chronic-Phase / therapy. Mycophenolic Acid / analogs & derivatives
  • [MeSH-minor] Adult. Allopurinol / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Benzamides. Biomarkers, Tumor / analysis. Case Management. Combined Modality Therapy. Drug Therapy, Combination. Fusion Proteins, bcr-abl / analysis. Fusion Proteins, bcr-abl / antagonists & inhibitors. Graft vs Host Disease / drug therapy. Graft vs Host Disease / etiology. Humans. Hydroxyurea / administration & dosage. Imatinib Mesylate. Immunosuppressive Agents / therapeutic use. Male. Piperazines / pharmacology. Piperazines / therapeutic use. Prednisone / therapeutic use. Pyrimidines / pharmacology. Pyrimidines / therapeutic use. Remission Induction. Thalidomide / therapeutic use. Transplantation Conditioning

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  • (PMID = 12053814.001).
  • [ISSN] 0034-8376
  • [Journal-full-title] Revista de investigación clínica; organo del Hospital de Enfermedades de la Nutrición
  • [ISO-abbreviation] Rev. Invest. Clin.
  • [Language] spa
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Benzamides; 0 / Biomarkers, Tumor; 0 / Immunosuppressive Agents; 0 / Piperazines; 0 / Pyrimidines; 4Z8R6ORS6L / Thalidomide; 63CZ7GJN5I / Allopurinol; 8A1O1M485B / Imatinib Mesylate; 9242ECW6R0 / mycophenolate mofetil; EC 2.7.10.2 / Fusion Proteins, bcr-abl; HU9DX48N0T / Mycophenolic Acid; VB0R961HZT / Prednisone; X6Q56QN5QC / Hydroxyurea
  • [Number-of-references] 25
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38. Chen Y, Peng C, Li D, Li S: Molecular and cellular bases of chronic myeloid leukemia. Protein Cell; 2010 Feb;1(2):124-32
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  • [Title] Molecular and cellular bases of chronic myeloid leukemia.
  • Chronic myeloid leukemia (CML) is a myeloproliferative disease characterized by the overproduction of granulocytes, which leads to high white blood cell counts and splenomegaly in patients.
  • Based on clinical symptoms and laboratory findings, CML is classified into three clinical phases, often starting with a chronic phase, progressing to an accelerated phase and ultimately ending in a terminal phase called blast crisis.
  • Blast crisis phase of CML is clinically similar to an acute leukemia; in particular, B-cell acute lymphoblastic leukemia (B-ALL) is a severe form of acute leukemia in blast crisis, and there is no effective therapy for it yet.
  • CML is induced by the BCR-ABL oncogene, whose gene product is a BCR-ABL tyrosine kinase.
  • Currently, inhibition of BCR-ABL kinase activity by its kinase inhibitor such as imatinib mesylate (Gleevec) is a major therapeutic strategy for CML.
  • However, the inability of BCR-ABL kinase inhibitors to completely kill leukemia stem cells (LSCs) indicates that these kinase inhibitors are unlikely to cure CML.
  • In addition, drug resistance due to the development of BCRABL mutations occurs before and during treatment of CML with kinase inhibitors.
  • A critical issue to resolve this problem is to fully understand the biology of LSCs, and to identify key genes that play significant roles in survival and self-renewal of LSCs.
  • In this review, we will focus on LSCs in CML by summarizing and discussing available experimental results, including the original studies from our own laboratory.
  • [MeSH-major] Fusion Proteins, bcr-abl / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Neoplastic Stem Cells / enzymology. Neoplastic Stem Cells / pathology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] 5-Lipoxygenase-Activating Proteins / metabolism. Animals. Benzamides. Disease Models, Animal. Humans. Imatinib Mesylate. Male. Mice. PTEN Phosphohydrolase / metabolism. Philadelphia Chromosome. Piperazines / therapeutic use. Point Mutation. Protein Structure, Tertiary. Pyrimidines / therapeutic use

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  • (PMID = 21203982.001).
  • [ISSN] 1674-8018
  • [Journal-full-title] Protein & cell
  • [ISO-abbreviation] Protein Cell
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 5-Lipoxygenase-Activating Proteins; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC4875160
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39. Mele L, Pagano L, Equitani F, Chiusolo P, Rossi E, Zini G, Teofili L, Leone G: Lymphoid blastic crisis in Philadelphia chromosome-positive chronic granulocytic leukemia following high-grade non-Hodgkin's lymphoma A case report and review of literature. Haematologica; 2000 May;85(5):544-8
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  • [Title] Lymphoid blastic crisis in Philadelphia chromosome-positive chronic granulocytic leukemia following high-grade non-Hodgkin's lymphoma A case report and review of literature.
  • In this paper we describe a case of a 65-year old man with a lymphoid blastic crisis of a chronic granulocytic leukemia occurring seven years after a palatine tonsillar non-Hodgkin's lymphoma treated with chemotherapy and radiation therapy.
  • The patient died within a few months, unresponsive to any treatment.
  • This is the first case, described in literature, of a secondary chronic granulocytic leukemia onset with a lymphoid blastic crisis.
  • [MeSH-major] Blast Crisis / etiology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications
  • [MeSH-minor] Aged. Bone Marrow Cells / pathology. Cytogenetics. Fatal Outcome. Fusion Proteins, bcr-abl / genetics. Humans. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / radiotherapy. Male. Neoplasms, Second Primary. Palatine Tonsil / pathology. Translocation, Genetic

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  • (PMID = 10800174.001).
  • [ISSN] 0390-6078
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] ITALY
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 40
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40. Thiele J, Kvasnicka HM, Schmitt-Graeff A, Schaefer HE: [Histologic and hematological findings in CML. A comparative immunohistochemical-morphometric and clinical study on bone marrow biopsies from 604 patients derived from two institutes of pathology (Cologne/Freiburg)]. Pathologe; 2000 Jan;21(1):39-54
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  • [Title] [Histologic and hematological findings in CML. A comparative immunohistochemical-morphometric and clinical study on bone marrow biopsies from 604 patients derived from two institutes of pathology (Cologne/Freiburg)].
  • [Transliterated title] Histologische und hämatologische Befunde bei der CML. Eine immunhistochemisch-morphometrische und klinische Vergleichsstudie an Beckenkammbiopsien von 604 Patienten aus zwei Instituten für Pathologie (Köln/Freiburg).
  • An immunohistochemical and morphometric study was performed on bone marrow biopsies in 604 patients with chronic myelogenous leukemia (CML) to compare morphological and clinical features and to evaluate effects of interferon (IFN) and chemotherapy.
  • Following morphometry significant correlations were calculated between number of CD61(+) megakaryocytes, including their precursors with fiber density.
  • This finding is in line with the close functional relationship between megakaryopoiesis and fibroblasts regarding the complex pathomechanism of myelofibrosis.
  • The latter was observed in about 28% of patients already at diagnosis.
  • In a similar way, the frequency of CD68(+) macrophages was correlated with the amount of Ret40f(+) nucleated erythroid precursors, implicating an involvement of this cell lineage in iron turnover, hemoglobin synthesis, and degradation of the expelled nuclei from normoblasts.
  • The (alpha-D-galactosyl residue-expressing) Pseudo-Gaucher cells were detectable in 30% of pretreatment specimens.
  • Moreover, significant associations were calculable between reduction in erythropoiesis or increase in fibers with clinical features such as hemoglobin level, percentages of myelo- and erythroblasts in the peripheral blood, and spleen size.
  • These variables are in keeping with more advanced stages of CML.
  • Based on our morphometric evaluations, a classification into three different histological subgroups: granulocytic, megakaryocytic, and myelofibrotic was carried out.
  • The dynamics of myelofibrosis and changes of major cell lineages during treatment were readily demonstrable by calculating corresponding indices.
  • These included the ratios between quantitative differences of corresponding variables at repeated examinations and time.
  • Thus, in patients with complete hematological remission following IFN administration, regeneration of erythropoiesis was found to be accompanied by an increase in the total number of CD68(+) macrophages, including activated subpopulations.
  • Histological subgroups showed a transition from a (nonfibrotic) granulocytic and megakaryocyte pattern to the myelofibrotic subtype in about 40% of patients.
  • This change was opposed to a numerical reduction in the myelofibrotic subtype which occurred in 17 patients (36%), but predominantly in those under HU therapy.
  • In conclusion, the striking heterogeneity of bone marrow features in CML warrants a careful morphological evaluation of trephine biopsies and appropriate means of processing to achieve relevant correlations with clinical data and, thus, allows a more elaborate insight into the dynamics of the disease process.
  • [MeSH-major] Bone Marrow / pathology. Hematopoietic Stem Cells / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • [MeSH-minor] Biopsy. Blood Cell Count. Bone Marrow Cells / cytology. Erythropoiesis. Humans. Immunohistochemistry. Macrophages / pathology. Reference Values. Retrospective Studies

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  • (PMID = 10663668.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] GERMANY
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41. Takahashi N, Miura I, Kobayashi Y, Kume M, Yoshioka T, Otane W, Ohtsubo K, Takahashi K, Kitabayashi A, Kawabata Y, Hirokawa M, Nishijima H, Ichinohasama R, Decoteau J, Miura AB, Sawada K: Fluorescence in situ hybridization monitoring of BCR-ABL-positive neutrophils in chronic-phase chronic myeloid leukemia patients during the primary stage of imatinib mesylate therapy. Int J Hematol; 2005 Apr;81(3):235-41
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  • [Title] Fluorescence in situ hybridization monitoring of BCR-ABL-positive neutrophils in chronic-phase chronic myeloid leukemia patients during the primary stage of imatinib mesylate therapy.
  • We describe a method for monitoring chronic myeloid leukemia (CML) patients treated with imatinib that uses fluorescence in situ hybridization (FISH) to detect BCR-ABL in peripheral blood (PB) granulocytes.
  • First, we compared this method, termed Neutrophil-FISH, with interphase FISH (i-FISH) analysis of bone marrow (BM), i-FISH analysis of PB mononuclear cells, and conventional cytogenetic analysis (CCA) of BM in 30 consecutive CML patients.
  • We found the percentage of BCR-ABL-positive neutrophils as determined by Neutrophil-FISH to correlate best with the percentage of Philadelphia chromosome-positive metaphases in the BM determined by CCA (y = 0.8818x + 5.7249; r(2) = 0.968).
  • We then performed a serial Neutrophil-FISH study of 10 chronic-phase CML patients treated with imatinib and found that the technique could clearly separate imatinib responders from nonresponders within 12 weeks of drug administration.
  • There was a significant difference in the percentages of BCR-ABL-positive neutrophils between responder (mean 3 SD, 18.2% 3 11.8%) and nonresponder (82.4% 3 5.1%) groups at 12 weeks (P < .0001, Student t test).Together with real-time quantitative polymerase chain reaction analysis, Neutrophil-FISH represents another useful method for monitoring CML patients during the primary myelosuppressive stage of imatinib therapy because it is a quick, simple, and reliable method for assessing cytogenetic response.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Fusion Proteins, bcr-abl / biosynthesis. In Situ Hybridization. Leukemia, Myeloid, Chronic-Phase / physiopathology. Neutrophils / metabolism. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Benzamides. Female. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / physiopathology. Male. Monitoring, Physiologic / methods

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  • (PMID = 15814334.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Japan
  • [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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42. Ramamoorthy SK, Pandita R, Prakash A, Ramaswamy NV, Al Bahar S: Safety of imatinib in chronic myeloid leukemia in blastic crisis presenting as cholestatic jaundice. Acta Haematol; 2007;118(3):141-5
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  • [Title] Safety of imatinib in chronic myeloid leukemia in blastic crisis presenting as cholestatic jaundice.
  • Acute leukemia presenting as cholestatic jaundice is rare.
  • It can occur due to granulocytic sarcoma compressing the bile ducts in case of acute myeloid leukemia.
  • We report a case of chronic myeloid leukemia in lymphoid blast cell crisis presenting with severe cholestatic jaundice due to diffuse infiltration of the liver sinusoids with lymphoblasts.
  • This patient tolerated imatinib well and, coinciding with the hematological response, there was marked reduction in the cholestasis due to blast clearance from the hepatic sinusoids.
  • He was subsequently treated with combination chemotherapy and achieved morphological and cytogenetic remission.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Blast Crisis / drug therapy. Jaundice, Obstructive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Liver Neoplasms / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Adult. Benzamides. Diagnosis, Differential. Drug-Related Side Effects and Adverse Reactions. Humans. Imatinib Mesylate. Male


43. Nuamah NM, Goker H, Kilic YA, Dagmoura H, Cakmak A: Spontaneous splenic rupture in a healthy allogeneic donor of peripheral-blood stem cell following the administration of granulocyte colony-stimulating factor (g-csf). A case report and review of the literature. Haematologica; 2006 May;91(5 Suppl):ECR08
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  • [Title] Spontaneous splenic rupture in a healthy allogeneic donor of peripheral-blood stem cell following the administration of granulocyte colony-stimulating factor (g-csf). A case report and review of the literature.
  • Human granulocyte colony-stimulating factor (G-CSF) is a hematopoietic hormone promoting the growth, proliferation, differentiation and maturation of myeloid and leukocytic lineages.
  • G-csfs have been used to improve granulocyte count in neutropenic patients, reduce the incidence and duration of neutropenia in patients receiving cytotoxic chemotherapy and to mobilize peripheral blood stem cells prior to leukapheresis for using in both autologous and allogeneic hematopoietic cell transplantation.
  • We herein, report a case of spontaneous splenic rupture secondary to high-dose G-CSF use (20 mcg/kg/day), in a healthy female allogeneic donor of peripheral-blood stem cell (PBSC) .
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / adverse effects. Hematopoietic Stem Cell Mobilization / adverse effects. Living Donors. Peripheral Blood Stem Cell Transplantation. Splenic Rupture / etiology
  • [MeSH-minor] Abdominal Pain / etiology. Adult. Female. Filgrastim. Hemoperitoneum / etiology. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Male. Recombinant Proteins. Rupture, Spontaneous. Splenectomy. Splenomegaly / chemically induced

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  • (PMID = 16709516.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; PVI5M0M1GW / Filgrastim
  • [Number-of-references] 20
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44. Vlasveld LT, Bos GM, Ermens AA, Bakker JA, Lindemans J: Hyperhomocysteinemia and functional cobalamin deficiency due to granulocytosis-induced alterations in the cobalamin-binding protein. Haematologica; 2006 Mar;91(3):394-6
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  • [Title] Hyperhomocysteinemia and functional cobalamin deficiency due to granulocytosis-induced alterations in the cobalamin-binding protein.
  • Serum cobalamin and homocysteine levels were studied in patients with chronic myelogenous leukemia (CML) and in stem cell donors treated with granulocyte-colony stimulating factor (G-CSF).
  • Cytoreductive treatment in patients with CML resulted in a decrease of cobalamin and homocysteine levels.
  • In stem cell donors cobalamin and homocysteine levels increased after G-CSF administration.
  • The increase of homocysteine level was accompanied by a decrease in the serum levels of the cobalamin-binding protein transcobalamin.
  • We hypothesize that the increased homocysteine levels in patients with CML and donors treated with G-CSF may be the result of a functional methylcobalamin deficiency due to decreased transcobalamin levels.
  • [MeSH-major] Hyperhomocysteinemia / blood. Transcobalamins / metabolism. Vitamin B 12. Vitamin B 12 Deficiency / blood
  • [MeSH-minor] Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy

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  • (PMID = 16531264.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Transcobalamins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; BR1SN1JS2W / mecobalamin; P6YC3EG204 / Vitamin B 12
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