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1. Radujkovic A, Topaly J, Fruehauf S, Zeller WJ: Combination treatment of imatinib-sensitive and -resistant BCR-ABL-positive CML cells with imatinib and farnesyltransferase inhibitors. Anticancer Res; 2006 May-Jun;26(3A):2169-77
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  • [Title] Combination treatment of imatinib-sensitive and -resistant BCR-ABL-positive CML cells with imatinib and farnesyltransferase inhibitors.
  • BACKGROUND: Resistance to imatinib monotherapy frequently emerges in advanced stages of chronic myelogenous leukemia (CML), supporting the rationale for combination drug therapy.
  • In the present study, the activities of the farnesyltransferase inhibitors (FTIs) L744,832 and LB42918, as single agents and in combination with imatinib, were investigated in different imatinib-sensitive and -resistant BCR-ABL-positive CML cells.
  • Drug interactions were analyzed according to the median-effect method of Chou and Talalay.
  • In primary chronic phase CML cells, additive and synergistic effects were discernible for the combination of imatinib plus L744,832 and imatinib plus LB42918, respectively.
  • Annexin V/propidium iodide staining showed enhancement of imatinib-induced apoptosis with either drug combination, both in imatinib-sensitive and -resistant cells.
  • CONCLUSION: The results indicated the potential of L744,832 and LB42918 as combination agents for CML patients on imatinib treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Enzyme Inhibitors / pharmacology. Farnesyltranstransferase / antagonists & inhibitors. Fusion Proteins, bcr-abl / biosynthesis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Benzamides. Cell Growth Processes / drug effects. Cell Line, Tumor. Humans. Imatinib Mesylate. K562 Cells. Methionine / administration & dosage. Methionine / analogs & derivatives. Methionine / pharmacology. P-Glycoprotein / metabolism. Piperazines / administration & dosage. Pyrimidines / administration & dosage

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  • (PMID = 16827161.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / L 744832; 0 / P-Glycoprotein; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; AE28F7PNPL / Methionine; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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2. Fischer T, Reifenrath C, Hess GR, Corsetti MT, Kreil S, Beck J, Meinhardt P, Beltrami G, Schuch B, Gschaidmeier H, Hehlmann R, Hochhaus A, Carella A, Huber C: Safety and efficacy of STI-571 (imatinib mesylate) in patients with bcr/abl-positive chronic myelogenous leukemia (CML) after autologous peripheral blood stem cell transplantation (PBSCT). Leukemia; 2002 Jul;16(7):1220-8
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  • [Title] Safety and efficacy of STI-571 (imatinib mesylate) in patients with bcr/abl-positive chronic myelogenous leukemia (CML) after autologous peripheral blood stem cell transplantation (PBSCT).
  • We examined safety and efficacy of STI-571 in 24 bcr/abl-positive patients with CML post PBSCT.
  • At start of STI-571 therapy, nine patients presented in blast crisis (BC) or in accelerated phase (AP), and 15 in chronic phase (CP).
  • In general, STI-571 was well tolerated in this heavily pretreated group of patients with a non-hematologic and hematologic toxicity profile similar to that observed in a previous phase I trial at comparable doses.
  • Five of nine patients with CML in transformation (AP, BC) were evaluable for hematologic response.
  • In CML chronic phase, STI-571 induced complete hematologic responses in all patients and major cytogenetic responses in 61% of patients with a complete cytogenetic response rate of 46%.
  • This report indicates that STI-571 is a safe and effective drug in heavily pretreated patients.
  • The high rate of complete hematologic and complete cytogenetic responses in CP patients is remarkable, as intensive treatment approaches plus IFN-alpha failed to be efficient in achieving long-term stabilization of CML in this patient cohort.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Fusion Proteins, bcr-abl / antagonists & inhibitors. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Adult. Benzamides. Blood Cell Count. Combined Modality Therapy. Enzyme Inhibitors / administration & dosage. Enzyme Inhibitors / adverse effects. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Protein-Tyrosine Kinases / antagonists & inhibitors. Transplantation, Autologous. Treatment Outcome

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  • (PMID = 12094246.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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3. von Bubnoff N, Duyster J: Chronic myelogenous leukemia: treatment and monitoring. Dtsch Arztebl Int; 2010 Feb;107(7):114-21
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  • [Title] Chronic myelogenous leukemia: treatment and monitoring.
  • BACKGROUND: The treatment options for bcr-abl positive chronic myelogenous leukemia (CML) include chemotherapy, immune therapy, allogeneic stem cell transplantation, and molecular therapy.
  • The tyrosine kinase inhibitor imatinib was approved for the treatment of CML in 2002.
  • Data from clinical trials allow a comparison of treatment options.
  • METHODS: The literature on the treatment and monitoring of CML was selectively reviewed.
  • RESULTS: In a clinical phase 3 trial of imatinib treatment for patients in the chronic phase of CML, the rates of progression-free and overall survival at 6 years were 93% and 88%, respectively.
  • One in four patients in the chronic phase of CML has an inadequate cytogenetic response to imatinib and therefore requires a change of treatment.
  • Most imatinib-resistant patients in the chronic phase of CML go into remission again after switching to one of the new tyrosine kinase inhibitors, dasatinib and nilotinib.
  • CONCLUSION: Imatinib is now the standard initial first-line treatment for CML in the chronic phase.
  • Regular hematologic and cytogenetic monitoring during treatment is indispensable so that patients with an inadequate response can be identified.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / mortality. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Stem Cell Transplantation / mortality. Stem Cell Transplantation / statistics & numerical data
  • [MeSH-minor] Benzamides. Humans. Imatinib Mesylate. Prevalence. Risk Assessment. Risk Factors. Survival Analysis. Survival Rate. Treatment Outcome

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  • (PMID = 20221270.001).
  • [ISSN] 1866-0452
  • [Journal-full-title] Deutsches Ärzteblatt international
  • [ISO-abbreviation] Dtsch Arztebl Int
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 98
  • [Other-IDs] NLM/ PMC2835925
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4. 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.
  • Bone marrow cytogenetic study demonstrated the presence of the typical t(9;22)(q34;q11) and the molecular biology study showed the p210 rearrangement (b2a2).
  • 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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5. Beham-Schmid C, Apfelbeck U, Sill H, Tsybrovsky O, Höfler G, Haas OA, Linkesch W: Treatment of chronic myelogenous leukemia with the tyrosine kinase inhibitor STI571 results in marked regression of bone marrow fibrosis. Blood; 2002 Jan 1;99(1):381-3
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  • [Title] Treatment of chronic myelogenous leukemia with the tyrosine kinase inhibitor STI571 results in marked regression of bone marrow fibrosis.
  • Morphologic bone marrow changes in patients with BCR-ABL-positive chronic myelogenous leukemia (CML) were investigated during treatment with the tyrosine kinase inhibitor STI571.
  • Bone marrow trephine biopsy specimens from 23 pretreated patients with CML were examined morphologically and by morphometry before and 6 weeks and 3 months after the initiation of STI571 therapy (Glivec, Novartis, Basel, Switzerland).
  • Bone marrow changes during treatment showed a quantitative normalization of erythropoiesis, a marked reduction of granulopoiesis, and a significant decrease in megakaryocytes with the reappearance of normal-sized forms.
  • These results may expand the profile of STI571 and may offer novel therapeutic possibilities in diseases with bone marrow fibrosis.
  • [MeSH-major] Enzyme Inhibitors / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / therapeutic use. Primary Myelofibrosis / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / therapeutic use. Benzamides. Biopsy. Bone Marrow / pathology. Erythropoiesis. Female. Granulocytes / pathology. Hematopoiesis. Humans. Imatinib Mesylate. Male. Megakaryocytes / pathology. Middle Aged. Remission Induction

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  • (PMID = 11756197.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
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6. Williams RT, Roussel MF, Sherr CJ: Arf gene loss enhances oncogenicity and limits imatinib response in mouse models of Bcr-Abl-induced acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2006 Apr 25;103(17):6688-93
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  • [Title] Arf gene loss enhances oncogenicity and limits imatinib response in mouse models of Bcr-Abl-induced acute lymphoblastic leukemia.
  • Mouse bone marrow cells transduced with retroviral vectors encoding either of two oncogenic Bcr-Abl isoforms (p210(Bcr-Abl) and p185(Bcr-Abl)) induce B cell lympholeukemias when transplanted into lethally irradiated mice.
  • When mouse bone marrow cells expressing Bcr-Abl are placed in short-term cultures selectively designed to support the outgrowth of pre-B cells, only those lacking one or two Arf alleles can initiate lympholeukemias when inoculated into immunocompetent, syngeneic recipient mice.
  • Although the ABL kinase inhibitor imatinib mesylate (Gleevec) provides highly effective treatment for BCR-ABL-positive chronic myelogenous leukemia, it has proven far less efficacious in the treatment of BCR-ABL-positive acute lymphoblastic leukemias (ALLs), many of which sustain deletions of the INK4A-ARF (CDKN2A) tumor suppressor locus.
  • Mice receiving Arf-/- or Arf+/- p210(Bcr-Abl)-positive pre-B cells do not achieve remission when maintained on high doses of oral imatinib therapy and rapidly succumb to lympholeukemia.
  • Although cells expressing the Bcr-Abl kinase can proliferate in the absence of IL-7, they remain responsive to this cytokine, which can reduce their sensitivity to imatinib.
  • Treatment of Arf-/-, p210(Bcr-Abl)-positive pre-B cells with imatinib together with an inhibitor of JAK kinases abrogates this resistance, suggesting that this combination may prove beneficial in the treatment of BCR-ABL-positive acute lymphoblastic leukemia.

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  • (PMID = 16618932.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA070089; United States / NCI NIH HHS / CA / P01 CA071907; United States / NCI NIH HHS / CA / T32-CA70089; United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA-71907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Cdkn2a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Interleukin-7; 0 / Piperazines; 0 / Pyrimidines; 0 / Tumor Suppressor Protein p14ARF; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC1440588
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7. 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.
  • 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.

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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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8. Topaly J, Zeller WJ, Fruehauf S: Synergistic activity of the new ABL-specific tyrosine kinase inhibitor STI571 and chemotherapeutic drugs on BCR-ABL-positive chronic myelogenous leukemia cells. Leukemia; 2001 Mar;15(3):342-7
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  • [Title] Synergistic activity of the new ABL-specific tyrosine kinase inhibitor STI571 and chemotherapeutic drugs on BCR-ABL-positive chronic myelogenous leukemia cells.
  • The ABL-specific tyrosine kinase inhibitor STI571 (formerly CGP57148B) induced cytogenetic remissions in 33% of chronic myelogenous leukemia (CML) patients in a phase I trial (Druker et al 1999).
  • Combination therapy may increase this proportion.
  • We tested whether combinations of STI571 and cytarabine or other chemotherapeutic agents such as hydroxyurea, mafosfamide or etoposide would display synergistic activity in BCR-ABL-positive chronic myelogenous leukemia (CML) cell lines derived from patients in blast crisis.
  • In addition, the toxicity of these combinations on BCR-ABL-negative cells was investigated.
  • The drug interactions were analyzed using the median-effect method of Chou and Talalay.
  • At growth inhibition levels of over 50%, STI571 + cytarabine as well as STI571 + etoposide were significantly synergistic (CI < 1, P < 0.05) in the BCR-ABL-positive cell lines evaluated.
  • At 60% inhibition or higher, a similar synergistic pattern became apparent for STI571 + mafosfamide (P < 0.05), while STI571 + hydroxyurea showed ambiguous, cell line-dependent synergism (BV173), additivity (EM-3) or antagonism (K562) in CML cell lines.
  • Furthermore, the BCR-ABL-negative HL-60, KG1a and normal CD34+ progenitor cells were not affected by 0.8 microM STI571, a concentration which produced more than 50% growth inhibition in all BCR-ABL-positive cells tested, and no potentiation of growth inhibition was observed in these BCR-ABL-negative cells when STI571 was combined with chemotherapeutic agents.
  • Our in vitro data with CML blast crisis cell lines strongly suggest that combinations of STI571 with cytarabine or etoposide be rapidly considered for clinical testing.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Enzyme Inhibitors / pharmacology. Fusion Proteins, bcr-abl / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / pharmacology
  • [MeSH-minor] Benzamides. Cytarabine / administration & dosage. Dose-Response Relationship, Drug. Drug Synergism. Humans. Hydroxyurea / administration & dosage. Imatinib Mesylate. Remission Induction

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  • (PMID = 11237055.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 04079A1RDZ / Cytarabine; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; X6Q56QN5QC / Hydroxyurea
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9. Schultheis B, Heissig B, Pasternak G, Hörner S, Hehlmann R: Interferon-alpha-treated patients with chronic myelogenous leukemia show BCR/ABL-positive peripheral blood progenitor cells surviving long-term culture. Folia Biol (Praha); 2000;46(6):251-5
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  • [Title] Interferon-alpha-treated patients with chronic myelogenous leukemia show BCR/ABL-positive peripheral blood progenitor cells surviving long-term culture.
  • Several groups have shown that Ph-progenitors reappear in LTC of CML bone marrow or PBMNC when the cell preparations were derived from newly diagnosed Ph-positive patients or after induction chemotherapy.
  • We have tested the hypothesis whether LTC may further decrease CML progenitors if the cells to be cultured were from IFN-treated patients.
  • In our experiments, PBMNC were cultured from 7 IFN- and 5 HU-treated patients in stable chronic phase of the disease, and from 9 patients at diagnosis.
  • Progenitor cells in PBMNC were quantitatively analyzed before and after 35 days of LTC by combining the clonogenic assay in semisolid medium with dual-color interphase FISH for identification of the BCR/ABL status of colony-forming progenitor cells.
  • A median of 22 colonies (range 7-88) before and 30 colonies (5-71) after LTC were analyzed per patient.
  • Our results show that the number of BCR/ABL-positive CFC before and after LTC was approximately the same.
  • This was independent of IFN or HU therapy.
  • In the IFN group there were 58% (median) BCR/ABL-positive CFC before and 54% (median) after LTC of PBMNC.
  • In the HU group, 80% of CFC were BCR/ABL-positive before and 85% after LTC.
  • A complete elimination of BCR/ABL-positive cells was not achieved.
  • We conclude that CML early progenitors in PBMNC of IFN-treated CML patients may survive LTC.
  • [MeSH-major] Biomarkers, Tumor / blood. Fusion Proteins, bcr-abl / blood. Immunologic Factors / therapeutic use. Interferon-alpha / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Neoplastic Cells, Circulating
  • [MeSH-minor] Antineoplastic Agents, Alkylating / therapeutic use. Humans. Hydroxyurea / therapeutic use. In Situ Hybridization, Fluorescence. Leukemia, Myeloid, Chronic-Phase / blood. Leukemia, Myeloid, Chronic-Phase / drug therapy. Leukemia, Myeloid, Chronic-Phase / genetics. Leukemia, Myeloid, Chronic-Phase / pathology. Neoplasm, Residual. Tumor Cells, Cultured. Tumor Stem Cell Assay

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  • (PMID = 11140858.001).
  • [ISSN] 0015-5500
  • [Journal-full-title] Folia biologica
  • [ISO-abbreviation] Folia Biol. (Praha)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Biomarkers, Tumor; 0 / Immunologic Factors; 0 / Interferon-alpha; EC 2.7.10.2 / Fusion Proteins, bcr-abl; X6Q56QN5QC / Hydroxyurea
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10. Moser AM, Manor E, Narkis G, Kapelushnik J: Imatinib resistant chronic myelogenous leukemia, BCR-ABL positive by chromosome and FISH analyses but negative by PCR, in a child progressing to acute basophilic leukemia: cytogenetic follow-up. Cancer Genet Cytogenet; 2006 Oct 1;170(1):54-7
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  • [Title] Imatinib resistant chronic myelogenous leukemia, BCR-ABL positive by chromosome and FISH analyses but negative by PCR, in a child progressing to acute basophilic leukemia: cytogenetic follow-up.
  • The case of an 11-year-old child with adult-type chronic myeloid leukemia, Philadelphia (BCR-ABL) positive, reverse transcription-polymerase chain reaction negative for the major, minor, and micro breakpoints is presented.
  • In the course of 3 years, the child failed to respond to treatment with hydroxyurea, refused all therapy for 6 months, was intolerant to alpha-interferon and progressed, while on imatinib, to acute basophilic leukemia.
  • A secondary cytogenetic clonal evolution, i(17q), developed during hydroxyurea treatment and a tertiary clonal evolution, +8, was detected during imatinib treatment.
  • It is not clear to what extent the several factors (undefined BCR-ABL breakpoint, treatment avoidance, and initial treatment choices, alone or in combination) played a role in the imatinib relapse and resistance and in the disease progression.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Genes, abl. Leukemia, Basophilic, Acute / surgery. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Bone Marrow Transplantation. Child. Disease Progression. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16965955.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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11. 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).
  • 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.
  • 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.
  • 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-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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12. Ross JS, Schenkein DP, Pietrusko R, Rolfe M, Linette GP, Stec J, Stagliano NE, Ginsburg GS, Symmans WF, Pusztai L, Hortobagyi GN: Targeted therapies for cancer 2004. Am J Clin Pathol; 2004 Oct;122(4):598-609
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  • [Title] Targeted therapies for cancer 2004.
  • The regulatory agency approvals in the United States and Europe of imatinib mesylate (Gleevec) for patients with bcr/abl-positive chronic myelogenous leukemia, cetuximab (Erbitux) for patients with epidermal growth factor receptor overexpressing metastatic colorectal cancer, the antiangiogenesis agent bevacizumab (Avastin), and the proteasome inhibitor bortezomib (Velcade)--and the considerable public interest in new anticancer drugs that take advantage of specific genetic defects that render the malignant cells more likely to respond to specific treatment--are driving a new era of integrated diagnostics and therapeutics.
  • The recent discovery of a drug response predicting activating mutation in the epidermal growth factor receptor gene for patients with non-small cell lung cancer treated with gefitinib (Iressa) has intensified this interest.
  • In this review, the history of targeted anticancer therapies is highlighted, with focus on the development of molecular diagnostics for hematologic malignancies and the emergence of trastuzumab (Herceptin), an antibody-based targeted therapy for HER-2/neu overexpressing metastatic breast cancer: The potential of pharmacogenomic strategies and the use of high-density genomic microarrays to classify and select therapy for cancer are briefly considered.
  • This review also considers the widely held view that, in the next 5 to 10 years, the clinical application of molecular diagnostics will further revolutionize the drug discovery and development process; customize the selection, dosing, route of administration of existing and new therapeutic agents; and truly personalize medical care for cancer patients.
  • [MeSH-major] Neoplasms / therapy
  • [MeSH-minor] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Bevacizumab. Breast Neoplasms / drug therapy. Cetuximab. Erlotinib Hydrochloride. Humans. Pharmacogenetics. Quinazolines / therapeutic use. Rituximab. Trastuzumab

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  • (PMID = 15487459.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Quinazolines; 0 / gemtuzumab; 0 / ibritumomab tiuxetan; 2S9ZZM9Q9V / Bevacizumab; 4F4X42SYQ6 / Rituximab; DA87705X9K / Erlotinib Hydrochloride; P188ANX8CK / Trastuzumab; PQX0D8J21J / Cetuximab; S65743JHBS / gefitinib
  • [Number-of-references] 132
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13. Merkerova M, Bruchova H, Brdicka R: Expression analysis of PCNA gene in chronic myelogenous leukemia--combined application of siRNA silencing and expression arrays. Leuk Res; 2007 May;31(5):661-72
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  • [Title] Expression analysis of PCNA gene in chronic myelogenous leukemia--combined application of siRNA silencing and expression arrays.
  • Imatinib metylase is the first choice treatment for BCR/ABL positive chronic myelogenous leukemia (CML).
  • However, as some CML patients develop resistance to imatinib therapy, there is a significant interest in development of alternative treatment strategies, such as identifying targets other than BCR/ABL that may participate in CML.
  • Previously, we demonstrated strong PCNA up-regulation in CML patients.
  • To further study its role in CML pathogenesis, we performed silencing of PCNA expression followed by array experiments.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Leukemic. Gene Silencing. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Oligonucleotide Array Sequence Analysis. Proliferating Cell Nuclear Antigen / genetics. RNA, Small Interfering / pharmacology
  • [MeSH-minor] Apoptosis. Benzamides. Biomarkers, Tumor / genetics. Cell Proliferation. Drug Resistance, Neoplasm. Fusion Proteins, bcr-abl / metabolism. Humans. Imatinib Mesylate. Piperazines / therapeutic use. Pyrimidines / therapeutic use. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured


14. 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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15. 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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16. 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).
  • 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.
  • 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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17. 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.
  • 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.
  • 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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18. Berger U, Engelich G, Maywald O, Pfirrmann M, Hochhaus A, Reiter A, Metzgeroth G, Gnad U, Hasford J, Heinze B, Heimpel H, Hossfeld DK, Kolb HJ, Löffler H, Pralle H, Queisser W, Hehlmann R, German CML-Study Group: Chronic myeloid leukemia in the elderly: long-term results from randomized trials with interferon alpha. Leukemia; 2003 Sep;17(9):1820-6
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  • [Title] Chronic myeloid leukemia in the elderly: long-term results from randomized trials with interferon alpha.
  • Chronic myeloid leukemia (CML) in older patients has not been studied well.
  • To assess the long-term outcome of older patients with Philadelphia- and/or BCR-ABL-positive CML, 199 patients aged >/=60 years representing 23% of 856 patients enrolled in the German randomized CML-studies I (interferon alpha (IFN) vs hydroxyurea (HU) vs busulfan (BU) and II (IFN+HU vs HU alone) were analyzed after a median observation time of 7 years.
  • Whereas 5-year survival in chemotherapy-treated older patients was inferior to that in younger patients (33 vs 46%, P=0.006 for HU and 29 vs 38%, P=0.042 for Bu), no significant survival difference could be verified in IFN-treated patients (46 vs 53%, P=0.077).
  • Adverse effects of IFN were similar in both age groups, but IFN dosage to achieve treatment goals was lower in older patients.
  • We conclude that the course of CML is not different in the elderly.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Interferon-alpha / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Busulfan / therapeutic use. Child. Female. Follow-Up Studies. Fusion Proteins, bcr-abl. Humans. Hydroxyurea / therapeutic use. Leukocyte Count. Male. Middle Aged. Prognosis. Randomized Controlled Trials as Topic. Risk. Survival Rate. Treatment Outcome

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  • (PMID = 12970782.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; G1LN9045DK / Busulfan; X6Q56QN5QC / Hydroxyurea
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19. Haus O, Kotlarek-Haus S, Makowska I, Duszeńko E, Jaźwiec B, Kuliczkowski K: [Cytogenetic changes in Ph(+) chronic granulocytic leukemia under the influence of interferon alpha (IFN-alpha) therapy]. Pol Arch Med Wewn; 2000 Jan-Feb;103(1-2):15-22
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  • [Title] [Cytogenetic changes in Ph(+) chronic granulocytic leukemia under the influence of interferon alpha (IFN-alpha) therapy].
  • Chromosomal changes during therapy with IFN-alpha were analysed in 21 patients suffering of chronic granulocytic leukemia.
  • In 6 persons additional chromosomal aberrations were present at diagnosis or during the disease course.
  • They disappeared on IFN-alpha therapy.
  • This fact may be in favour of the influence of IFN-alpha not only on disappearance of Ph chromosome, but also of secondary aberrations, some of them indicating the possibility of an acceleration of the disease.
  • No relation of the CgR, as well as Sokal index value to the survival time in presented small cohort could be observed, which may depend on short observation time.
  • CgR did not depend on a type of fusion of BCR/ABL gene.
  • However, survival time was longer in patients with b3a2 fusion.
  • [MeSH-major] Chromosome Aberrations. Interferon-alpha / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Philadelphia Chromosome

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  • (PMID = 11236254.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Interferon-alpha
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20. 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.
  • 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


21. Liu WM, Lawrence AJ, Joel SP: The importance of drug scheduling and recovery phases in determining drug activity. Improving etoposide efficacy in BCR-ABL-positive CML cells. Eur J Cancer; 2002 Apr;38(6):842-50
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  • [Title] The importance of drug scheduling and recovery phases in determining drug activity. Improving etoposide efficacy in BCR-ABL-positive CML cells.
  • We have investigated the effect of etoposide schedule on cell cycle distribution, apoptosis and p21(waf1) and cdk1(p34) status in two bcr-abl-positive chronic myeloid leukaemia (CML) cell lines (K562 and KU812) and two small cell lung cancer (SCLC) cell lines (H69 and GLC4).
  • During a continuous 5-day exposure, the SCLC cell lines showed a time and concentration-dependent loss of cell viability, with an initial block in the G2/M phase of the cell cycle followed by apoptosis.
  • In contrast, the two CML cell lines showed no significant apoptosis or loss of viability after a similar block in G2/M.
  • However, when K562 or KU812 cells were placed in drug-free medium following a 3-day drug exposure there was marked, concentration-dependent apoptosis (% apoptosis after release at 1 microM etoposide in K562, 10% at 24 h, 30% at 48 h).
  • Our data also show that p21(waf1) does not increase after etoposide treatment in either H69 or GLC4 (both with mutated-p53).
  • Although K562 and KU812 cells are null-p53, the arrest in G2/M during drug exposure was associated with increased p21(waf1) and a decrease in cdk1 (both P<0.001 compared with controls).
  • Upon release of these cells from drug-medium, p21(waf1) gradually returned to control levels, which was associated with an easing of the block at G2/M and an induction of apoptosis.
  • This study highlights the importance of cell cycle regulatory proteins in drug sensitivity and resistance, and suggests that in cells such as K562 and KU812, a pulsed schedule may be more active than a single prolonged exposure.
  • [MeSH-major] Etoposide / administration & dosage. Fusion Proteins, bcr-abl / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • [MeSH-minor] CDC2 Protein Kinase / metabolism. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / metabolism. Dose-Response Relationship, Drug. Drug Administration Schedule. Flow Cytometry. G2 Phase. Humans. Immunoblotting. Tumor Cells, Cultured

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  • (PMID = 11937320.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 6PLQ3CP4P3 / Etoposide; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.22 / CDC2 Protein Kinase
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22. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • We evaluated gender, age, location, GS antedating leukemia, underlying disorders, treatment type and stem cell transplantation.
  • 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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23. Chen ZC, You Y, Zhu XM, Li QB, Li WM, Zou P: [A clinical study of treating 120 cases of adult chronic myelocytic leukemia with imatinib mesylate]. Zhonghua Nei Ke Za Zhi; 2007 Dec;46(12):1003-6
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  • [Title] [A clinical study of treating 120 cases of adult chronic myelocytic leukemia with imatinib mesylate].
  • OBJECTIVE: To analyze and evaluate the clinical efficacy and safety of imatinib mesylate (IM) as a tyrosine kinase inhibitor on Ph-positive or BCR/ABL positive chronic myelogenous leukemia (CML).
  • METHODS: 120 patients diagnosed as CML with positive Ph chromosome were treated with IM 400 mg/d for CML in chronic phase (CP) (n = 90) or 600 mg/d for CML in accelerated or blastic phase (AP or BP) (n = 30) once daily.
  • Hematological, cytogenetic and molecular effects of IM on the disease process of these patients were evaluated with blood and marrow cells morphology examination, G-band conventional cytogenetics analysis for Ph chromosome and PCR assay for BCR/ABL gene.
  • The treatment efficacy and safety were retrospectively studied. RESULTS:.
  • (1) In CML-CP patients, after a follow-up of 9 ( range 3-42) months, cumulative complete hematological response (CHR), complete cytogenetic response (CCyR) and complete molecular response (CMR) rates were 73.3%, 66.7% and 54.4%, which was not influenced by prior treatment of interferon.
  • CMR was better when time from diagnosis to treatment with IM was < or = 6 months (P < 0.05).
  • It is significant that the time to first CHR and time to first CCyR were related with the time to first CCyR and the time to first negative BCR/ ABL, respectively (both P < 0.05), while there was no relation between the time to first CHR and the time to first negative BCR/ABL (P > 0.05). (2) CHR, CCyR and CMR rates of the patients with progressive course (AP and BP) were 43.3%, 25.9% and 25.0%, respectively.
  • The total mortality rate was 30.0%. (3) The mortality rate of the patients with age < or = 25 was higher than those >25 (P < 0.05). (4) Grade 3 leukocytopenia occurred in 16.0% of the patients and grade 3 thrombocytopenia in 18.0% of the patients and they 12 (5-20) weeks and 9 (3-16) weeks after the treatment, respectively.
  • CONCLUSION: IM can lead to considerable hematological, cytogenetic and molecular response rates in CML, especially CML-CP patients, with minor tolerable side effects.
  • [MeSH-major] Leukemia, Myeloid, Chronic-Phase / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Benzamides. Female. Fusion Proteins, bcr-abl / genetics. Humans. Imatinib Mesylate. Male. Middle Aged. Philadelphia Chromosome. Retrospective Studies. Treatment Outcome

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  • (PMID = 18478917.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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24. 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.
  • 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.
  • [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


25. Mahon FX, Hayette S, Lagarde V, Belloc F, Turcq B, Nicolini F, Belanger C, Manley PW, Leroy C, Etienne G, Roche S, Pasquet JM: Evidence that resistance to nilotinib may be due to BCR-ABL, Pgp, or Src kinase overexpression. Cancer Res; 2008 Dec 1;68(23):9809-16
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  • [Title] Evidence that resistance to nilotinib may be due to BCR-ABL, Pgp, or Src kinase overexpression.
  • Targeting the tyrosine kinase activity of Bcr-Abl is an attractive therapeutic strategy in chronic myeloid leukemia (CML) and in Bcr-Abl-positive acute lymphoblastic leukemia.
  • Whereas imatinib, a selective inhibitor of Bcr-Abl tyrosine kinase, is now used in frontline therapy for CML, second-generation inhibitors of Bcr-Abl tyrosine kinase such as nilotinib or dasatinib have been developed for the treatment of imatinib-resistant or imatinib-intolerant disease.
  • Overexpression of BCR-ABL and multidrug resistance gene (MDR-1) were found among the investigated mechanisms.
  • Moreover, failure of nilotinib treatment was accompanied by an increase of Lyn mRNA expression in patients with resistant CML.
  • Two Src kinase inhibitors (PP1 and PP2) partially removed resistance but did not significantly inhibit Bcr-Abl tyrosine kinase activity.
  • In contrast, dasatinib, a dual Bcr-Abl and Src kinase inhibitor, inhibited the phosphorylation of both BCR-ABL and Lyn, and induced apoptosis of the Bcr-Abl cell line overexpressing p53/56 Lyn.
  • [MeSH-major] Fusion Proteins, bcr-abl / biosynthesis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. P-Glycoprotein / biosynthesis. Pyrimidines / pharmacology. src-Family Kinases / biosynthesis
  • [MeSH-minor] Antineoplastic Agents. Dasatinib. Drug Resistance, Neoplasm. Humans. K562 Cells. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Small Interfering / genetics. Thiazoles / pharmacology. Transfection


26. Kim J, Park CJ, Seo EJ, Lee JH, Yoo SJ, Choi SJ, Chi HS: A case of biphenotypic blast crisis of unclassified myeloproliferative disorder. Ann Hematol; 2002 Oct;81(10):603-4
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  • Since Ph chromosome and bcr-abl gene rearrangement were absent, the diagnosis of an unclassified MPD in the blast crisis phase was established.
  • The patient went into a complete remission after chemotherapy, but marked granulocytic hyperplasia (M:E ratio of 5.7) and 90% cellularity remained.
  • Blast crisis recurred during subsequent intensification chemotherapy and the patient did not go into a complete remission regardless of the intense chemotherapy.
  • The blast crisis transformed from unclassified MPD had a grave prognosis as it responded poorly to chemotherapy.
  • This unique blast crisis is distinguishable from the blast crisis of chronic myelogenous leukemia.
  • [MeSH-major] Blast Crisis / diagnosis. Myeloproliferative Disorders / pathology

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  • (PMID = 12424544.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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27. 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.
  • 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-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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28. Jagani Z, Song K, Kutok JL, Dewar MR, Melet A, Santos T, Grassian A, Ghaffari S, Wu C, Yeckes-Rodin H, Ren R, Miller K, Khosravi-Far R: Proteasome inhibition causes regression of leukemia and abrogates BCR-ABL-induced evasion of apoptosis in part through regulation of forkhead tumor suppressors. Cancer Res; 2009 Aug 15;69(16):6546-55
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  • [Title] Proteasome inhibition causes regression of leukemia and abrogates BCR-ABL-induced evasion of apoptosis in part through regulation of forkhead tumor suppressors.
  • BCR-ABL plays an essential role in the pathogenesis of chronic myeloid leukemia (CML) and some cases of acute lymphocytic leukemia (ALL).
  • Although ABL kinase inhibitors have shown great promise in the treatment of CML, the persistence of residual disease and the occurrence of resistance have prompted investigations into the molecular effectors of BCR-ABL.
  • Here, we show that BCR-ABL stimulates the proteasome-dependent degradation of members of the forkhead family of tumor suppressors in vitro, in an in vivo animal model, and in samples from patients with BCR-ABL-positive CML or ALL.
  • As several downstream mediators of BCR-ABL are regulated by the proteasome degradation pathway, we also show that inhibition of this pathway, using bortezomib, causes regression of CML-like disease.
  • Bortezomib treatment led to inhibition of BCR-ABL-induced suppression of FoxO proteins and their proapoptotic targets, tumor necrosis factor-related apoptosis-inducing ligand and BIM, thereby providing novel insights into the molecular effects of proteasome inhibitor therapy.
  • We additionally show sensitivity of imatinib-resistant BCR-ABL T315I cells to bortezomib.
  • Our data delineate the involvement of FoxO proteins in BCR-ABL-induced evasion of apoptosis and provide evidence that bortezomib is a candidate therapeutic in the treatment of BCR-ABL-induced leukemia.

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  • [ErratumIn] Cancer Res. 2009 Sep 1;69(17):7130. Rodin, Heather Yeckes [corrected to Yeckes-Rodin, Heather]
  • (PMID = 19654305.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL080192-05; United States / NHLBI NIH HHS / HL / HL080192; United States / NHLBI NIH HHS / HL / R01 HL080192; United States / NCI NIH HHS / CA / R01 CA131664; United States / NHLBI NIH HHS / HL / R01 HL080192-05; United States / NCI NIH HHS / CA / P30CA6516; United States / NCI NIH HHS / CA / R01 CA105306-05; United States / NCI NIH HHS / CA / R01 CA105306; United States / NCI NIH HHS / CA / CA105306; United States / NCI NIH HHS / CA / P30 CA006516; United States / NCI NIH HHS / CA / CA105306-05; United States / NCI NIH HHS / CA / CA131664
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Boronic Acids; 0 / Cysteine Proteinase Inhibitors; 0 / Forkhead Transcription Factors; 0 / Piperazines; 0 / Proteasome Inhibitors; 0 / Pyrazines; 0 / Pyrimidines; 0 / Tumor Suppressor Proteins; 69G8BD63PP / Bortezomib; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ NIHMS123965; NLM/ PMC2763358
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29. Greene LM, Kelly L, Onnis V, Campiani G, Lawler M, Williams DC, Zisterer DM: STI-571 (imatinib mesylate) enhances the apoptotic efficacy of pyrrolo-1,5-benzoxazepine-6, a novel microtubule-targeting agent, in both STI-571-sensitive and -resistant Bcr-Abl-positive human chronic myeloid leukemia cells. J Pharmacol Exp Ther; 2007 Apr;321(1):288-97
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  • [Title] STI-571 (imatinib mesylate) enhances the apoptotic efficacy of pyrrolo-1,5-benzoxazepine-6, a novel microtubule-targeting agent, in both STI-571-sensitive and -resistant Bcr-Abl-positive human chronic myeloid leukemia cells.
  • Interactions between the Bcr-Abl kinase inhibitor STI-571 (imatinib mesylate) and a novel microtubule-targeting agent (MTA), pyrrolo-1,5-benzoxazepine (PBOX)-6, were investigated in STI-571-sensitive and -resistant human chronic myeloid leukemia (CML) cells.
  • Cotreatment of PBOX-6 with STI-571 induced significantly more apoptosis in Bcr-Abl-positive CML cell lines (K562 and LAMA-84) than either drug alone (P < 0.01).
  • Cell cycle analysis of propidium iodide-stained cells showed that STI-571 significantly reduced PBOX-6-induced G2M arrest and polyploid formation with a concomitant increase in apoptosis.
  • Similar results were obtained in K562 CML cells using lead MTAs (paclitaxel and nocodazole) in combination with STI-571.
  • Potentiation of PBOX-6-induced apoptosis by STI-571 was specific to Bcr-Abl-positive leukemia cells with no cytoxic effects observed on normal peripheral blood cells.
  • The combined treatment of STI-571 and PBOX-6 was associated with the down-regulation of Bcr-Abl and repression of proteins involved in Bcr-Abl transformation, namely the antiapoptotic proteins Bcl-x(L) and Mcl-1.
  • Together, these findings highlight the potential clinical benefits in simultaneously targeting the microtubules and the Bcr-Abl oncoprotein in STI-571-sensitive and -resistant CML cells.
  • [MeSH-major] Apoptosis / drug effects. Fusion Proteins, bcr-abl / metabolism. Leukemia, Myeloid / drug therapy. Microtubules / drug effects. Oxazepines / pharmacology. Piperazines / pharmacology. Pyrimidines / pharmacology. Pyrroles / pharmacology
  • [MeSH-minor] Benzamides. Blotting, Western. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Down-Regulation / physiology. Drug Resistance, Neoplasm. Drug Synergism. HL-60 Cells. Humans. Imatinib Mesylate. K562 Cells. Monocytes / drug effects. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Poly(ADP-ribose) Polymerase Inhibitors. Poly(ADP-ribose) Polymerases / metabolism. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Proto-Oncogene Proteins c-bcl-2 / genetics. bcl-X Protein / biosynthesis. bcl-X Protein / genetics

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  • (PMID = 17202400.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Oxazepines; 0 / PBOX-6; 0 / Piperazines; 0 / Poly(ADP-ribose) Polymerase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrimidines; 0 / Pyrroles; 0 / bcl-X Protein; 8A1O1M485B / Imatinib Mesylate; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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30. Bright SA, Greene LM, Greene TF, Campiani G, Butini S, Brindisi M, Lawler M, Meegan MJ, Williams DC, Zisterer DM: The novel pyrrolo-1,5-benzoxazepine, PBOX-21, potentiates the apoptotic efficacy of STI571 (imatinib mesylate) in human chronic myeloid leukaemia cells. Biochem Pharmacol; 2009 Feb 1;77(3):310-21
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  • [Title] The novel pyrrolo-1,5-benzoxazepine, PBOX-21, potentiates the apoptotic efficacy of STI571 (imatinib mesylate) in human chronic myeloid leukaemia cells.
  • The Bcr-Abl kinase inhibitor, STI571, is the first line treatment for chronic myeloid leukaemia (CML), but the recent emergence of STI571 resistance has led to the examination of combination therapies.
  • In this report, we describe how a novel non-toxic G1-arresting compound, pyrrolo-1,5-benzoxazepine (PBOX)-21, potentiates the apoptotic ability of STI571 in Bcr-Abl-positive CML cells.
  • Co-treatment of CML cells with PBOX-21 and STI571 induced more apoptosis than either drug alone in parental (K562S and LAMA84) and STI571-resistant cells lines (K562R).
  • This potentiation of apoptosis was specific to Bcr-Abl-positive leukaemia cells with no effect observed on Bcr-Abl-negative HL-60 acute myeloid leukaemia cells.
  • Apoptosis induced by PBOX-21/STI571 resulted in activation of caspase-8, cleavage of PARP and Bcl-2, upregulation of the pro-apoptotic protein Bim and a downregulation of Bcr-Abl.
  • Repression of proteins involved in Bcr-Abl transformation, the anti-apoptotic proteins Mcl-1 and Bcl-(XL) was also observed.
  • Apoptosis was significantly reduced following pre-treatment with either the general caspase inhibitor Boc-FMK or the chymotrypsin-like serine protease inhibitor TPCK, but was completely abrogated following pre-treatment with a combination of these inhibitors.
  • In conclusion, our data highlights the potential of PBOX-21 in combination with STI571 as an effective therapy against CML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Carbamates / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Oxazepines / therapeutic use. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Blotting, Western. Cell Line, Tumor. Down-Regulation. Drug Synergism. Flow Cytometry. Fusion Proteins, bcr-abl / metabolism. Humans. Imatinib Mesylate. Membrane Potentials / drug effects. Up-Regulation

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  • (PMID = 19014913.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 7-((diethylcarbamoyl)oxy)-6-p-tolylpyrrolo(2,1-d)(1,5)benzoxazepine; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Carbamates; 0 / Oxazepines; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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31. 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.
  • Cytogenetic analysis showed an abnormal karyotype with rearrangement of chromosomes 4 and 22.
  • PCR amplification and subsequent sequence analysis demonstrated an in-frame 5'-BCR/3'-PDGFRA fusion in the patient's cDNA.
  • 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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32. 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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  • 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).
  • The expression levels of bcr/abl and bcl-2 gene were reduced by IFN-alpha or IFN-alpha plus IL-6.
  • 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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33. Stuart SA, Minami Y, Wang JY: The CML stem cell: evolution of the progenitor. Cell Cycle; 2009 May 1;8(9):1338-43
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  • [Title] The CML stem cell: evolution of the progenitor.
  • The success of imatinib mesylate (STI571, Gleevec) in treating chronic myeloid leukemia (CML) is, to date, the crowning achievement of targeted molecular therapy in cancer.
  • Nearly 90% of newly diagnosed patients treated with imatinib in the chronic phase of the disease achieve a complete cytogenetic response.
  • However, more than 95% of these patients retain detectable levels of BCR-ABL mRNA and patients discontinuing imatinib therapy almost invariably relapse, demonstrating that an imatinib insensitive population of leukemia-initiating cells (LICs) persists in nearly all patients.
  • These findings underscore the need for treatments specifically targeting the leukemia-initiating population of CML cells.
  • While mounting evidence suggests that the LIC in the chronic phase of CML is the BCR-ABL positive hematopoietic stem cell, several recent publications suggest that during CML blast crisis, a granulocyte-macrophage progenitor (GMP) population also acquires LIC properties through activation of the beta-catenin pathway.
  • Characterization of these cells and evaluation of their sensitivity to imatinib is critical to our understanding and treatment of CML blast crisis.

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  • (PMID = 19342894.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA043054-23; United States / NCI NIH HHS / CA / R01 CA043054; United States / NCI NIH HHS / CA / T32 CA067754; United States / NCI NIH HHS / CA / R01 CA043054-23
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ NIHMS159789; NLM/ PMC2792634
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34. 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).
  • 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.
  • Apoptosis assay by the mono-oligonucleosome detection and acridine orange/propidium iodide dye revealed marked apoptosis underlying cytotoxicity.
  • [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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35. Fischer T: [Results up to now of administration of STI-571 (Glivec) in recurrence after allogenic and autologous stem cell transplantation in chronic myeloid leukemia]. Med Klin (Munich); 2002 Jan 15;97 Suppl 1:22-7
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  • [Title] [Results up to now of administration of STI-571 (Glivec) in recurrence after allogenic and autologous stem cell transplantation in chronic myeloid leukemia].
  • [Transliterated title] Bisherige Ergebnisse beim Einsatz von STI-571 (Glivec) im Rezidiv nach allogener bzw. autologer Stammzelltransplantation bei CML.
  • BACKGROUND: Gleevec (STI-571) is s selective inhibitor of the bcr/abl tyrosine kinase.
  • Recent phase I and phase II studies in patients with bcr/abl positive CML and ALL showed a low rate of grade III/IV toxicity and good clinical efficacy.
  • THERAPY AND RESULTS: 18 of 18 patients with cytogenetic and/or hematologic relapse in chronic phase CML post autologous stem cell transplantation achieved a complete hematologic remission upon therapy with Gleevec.
  • The cytogenetic response rate was 75% with a complete cytogenetic response rate of 50%.
  • After allogeneic stem cell transplantation, patients in cytogenetic or hematologic relapse also experienced high hematologic and cytogenetic response rates upon therapy with Gleevec.
  • No symptoms of chronic extensive or > grade I acute GvHD could be observed.
  • Grade III/IV granulocytopenia and/or thrombopenia could be observed in 50% of patients with transformed phases of CML.
  • CONCLUSION: These results show a new approach in treatment of patients with Philadelphia-chromosome-positive leukemia relapsing post autologous or allogeneic stem cell transplantation.
  • The data suggest that early start of STI-571 therapy in MRD-positive patients is a promising approach.
  • Recently, a multicenter phase II study to evaluate the toxicity and efficacy of Gleevec in CML patients with minimal residual disease post allogeneic transplantation was started.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Benzamides. Child. Clinical Trials as Topic. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Remission Induction. Treatment Outcome


36. Burchert A: Roots of imatinib resistance: a question of self-renewal? Drug Resist Updat; 2007 Aug-Oct;10(4-5):152-61
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  • The BCR-ABL-fusion gene is critical for the development of chronic myeloid leukemia (CML) and BCR-ABL positive acute lymphatic leukemia (Ph+ ALL).
  • Blocking BCR-ABL by the ABL tyrosine kinase inhibitor imatinib mesylate (IM, Gleevec) is clinically highly efficient.
  • Treatment response is unfortunately compromised by the emergence of IM resistance, which is regularly seen in accelerated and blastic phase of CML (CML-AP/BP) and in Ph+ ALL.
  • BCR-ABL kinase domain mutations are then considered the causative mechanism of IM resistance, because 50-60% of the IM resistant patients harbour such mutations.
  • In contrast, IM resistance arises very rarely in patients that are treated with IM in early chronic phase of CML.
  • This implies that BCR-ABL independent factors such as the cellular context of BCR-ABL expression and stage of disease decisively control the evolution of IM resistance.
  • In line with this, novel Abl-kinase inhibitors such as dasatinib (DA) or nilotinib (NI) - although capable of inhibiting most of the BCR/-BL kinase mutants - still often fail to overcome resistance and do mostly not induce durable cytogenetic responses in IM resistant CML-AP/BC and Ph+ ALL patients.
  • On the basis of available evidence it is proposed here that alternative genetic aberrations, which synergize with BCR-ABL to enable leukemic self-renewal are of causal importance for the evolution of clinical kinase inhibitor resistance.
  • This model has clinical implications as it implies that even highly potent Abl-kinase inhibition can not target the genetic basis of IM resistance and will also not resolve the problem of Abl-kinase inhibitor resistance.
  • [MeSH-major] Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Benzamides. Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Models, Biological. Mutation

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  • (PMID = 17683977.001).
  • [ISSN] 1368-7646
  • [Journal-full-title] Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy
  • [ISO-abbreviation] Drug Resist. Updat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 104
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37. 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.
  • The latter was observed in about 28% of patients already at diagnosis.
  • 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.
  • 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

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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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38. Huang HF, Chen YZ, Wu Y: [Effect of zinc phthalocyanine-mediated photodynamic therapy on bone marrow purging, an experimental study]. Zhonghua Yi Xue Za Zhi; 2003 Jun 10;83(11):986-91
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  • [Title] [Effect of zinc phthalocyanine-mediated photodynamic therapy on bone marrow purging, an experimental study].
  • OBJECTIVE: To probe into the purging effects of zinc phthalocyanine-mediated photodynamic therapy (PDT) on simulated remission bone marrow grafts of chronic granulocytic leukemia. METHODS:.
  • (1) K562 cells, aline chronic granulocytic leukemia cells, and normal mononuclear cells (MNC) were cultured.
  • Fluorescence spectrophotometry was used to determine the concentration of zinc phthalocyanine in cells at different time points so as to find the optimal time for photodynamic purging process. (2) Suspensions of K562 cells and MNCs were made and incubated with zinc phthalocyanine of different concentrations (0.062 5, 0.125, 0.25, 0.5, and 1.0 micro g/ml) for 5 hours.
  • After PDT treatment, colony formation test was done and nested-PCR was used to detect the bcr-abl mRNA expression in K562 cells.
  • However, the zinc phthalocyanine content in the K562 cells gradually increased within the first 4 hours of incubation and reached its peak by the fifth hour with a ratio of zinc phthalocyanine content in K562 cells to that in MNCs of 4.59.
  • Therefore, the fifth hour after incubation was selected as the optimal time to irradiate the suspensions using the laser with a wavelength of 670 nm. (2) The inhibitory rate of laser on the colony information rate was 91.1% for the K562 cells, 18.0% for the MNCs in CFU-Mix methyl cellulose culture system, 18.6% for the MNCs in CFU-GM methyl cellulose culture system, and 17.8% for the MNCs in CFU-E methyl cellulose culture system At the concentration of 0.25 micro g/ml, K562 cells were inhibited by 91.1%, however, CFU-Mix, CFU-GM and CFU-E were relatively spared, inhibitory rate being 18.0%, 18.6% and 17.8% respectively. (3) At the concentration of 0.25 micro g/ml, residual K562 cells in the simulated remission bone marrow were completely photoinactivated.
  • It would be a promising purging technique for chronic granulocytic leukemia.
  • [MeSH-minor] Cell Count. Hematopoietic Stem Cells / drug effects. Humans. K562 Cells

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  • (PMID = 12899802.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi 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 / Indoles; 0 / Organometallic Compounds; 14320-04-8 / Zn(II)-phthalocyanine
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39. Radojkovic M, Ristic S, Pavlovic S, Colovic M: Molecular response to imatinib in patient with Ph negative p190 BCR-ABL transcript positive chronic myeloid leukemia with cyclic leukocytosis. Leuk Res; 2009 Jun;33(6):e10-2
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  • [Title] Molecular response to imatinib in patient with Ph negative p190 BCR-ABL transcript positive chronic myeloid leukemia with cyclic leukocytosis.
  • An atypical case of Philadelphia (Ph) negative, e1a2 BCR-ABL transcript positive chronic myeloid leukemia (CML) characterized with cyclic periodic leukocytosis and spontaneous remissions is reported.
  • So far, only few Ph positive CML patients expressing p190 BCR-ABL protein and different clinical characteristics and treatment have been described in the literature.
  • This is the first report of Philadelphia negative, p190 BCR-ABL positive CML with cyclic spontaneous oscillation of white blood cell count (WBC), and excellent response to imatinib treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Genes, abl. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukocytosis. Piperazines / therapeutic use. Pyrimidines / therapeutic use. RNA, Messenger / genetics


40. Koldehoff M, Beelen DW, Trenschel R, Steckel NK, Peceny R, Ditschkowski M, Ottinger H, Elmaagacli AH: Outcome of hematopoietic stem cell transplantation in patients with atypical chronic myeloid leukemia. Bone Marrow Transplant; 2004 Dec;34(12):1047-50
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  • [Title] Outcome of hematopoietic stem cell transplantation in patients with atypical chronic myeloid leukemia.
  • Atypical chronic myeloid leukemia (aCML) occurs rarely and is associated with a poor prognosis when treated with conventional chemotherapy.
  • Analysis of the leukocyte chimerism of peripheral white blood cells and bone marrow buffy coat cells by VNTR-polymerase chain reaction (PCR) and single-nucleotide polymorphism real-time PCR revealed complete chimerism in all patients who had received an allogeneic transplant.
  • All other patients were alive at the time of analysis.
  • Our findings suggest that the outcome of allogeneic or syngeneic transplantation in patients with aCML may not be worse than the outcome of transplantation for BCR-ABL-positive CML.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy
  • [MeSH-minor] Adult. Female. Follow-Up Studies. Graft vs Host Disease. Humans. Male. Middle Aged. Opportunistic Infections. Remission Induction. Retrospective Studies. Tissue Donors. Transplantation Chimera. Transplantation, Homologous. Transplantation, Isogeneic. Treatment Outcome


41. 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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42. 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

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • Hazardous Substances Data Bank. HYDROXYUREA .
  • Hazardous Substances Data Bank. MYCOPHENOLATE MOFETIL .
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • Hazardous Substances Data Bank. Allopurinol .
  • Hazardous Substances Data Bank. THALIDOMIDE .
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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
  •  go-up   go-down


43. Rosário Cavalheiro Rde C, Vicari P, Maria Morselli F, Ommati LV, Frazão Rosa Fde O, Rodrigues Oliveira JS: Granulocytic sarcoma giant in chronic myeloid leukemia during imatinib mesylate therapy. Am J Hematol; 2006 Jan;81(1):76-7
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Granulocytic sarcoma giant in chronic myeloid leukemia during imatinib mesylate therapy.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Neoplasms, Second Primary / therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Sarcoma, Myeloid / therapy
  • [MeSH-minor] Adult. Benzamides. Combined Modality Therapy. Fatal Outcome. Female. Humans. Imatinib Mesylate






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