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


2. 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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3. 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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4. Thiele J, Kvasnicka HM, Schmitt-Graeff A, Cvetanovska G, Blum N, Schaefer HE: Therapy-related changes of CD20+ and CD45RO+ lymphocyte subsets in chronic myeloid leukemia (CML): an immunohistochemical and morphometric study on sequential trephine biopsies of the bone marrow. Mod Pathol; 2000 Aug;13(8):888-96
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  • [Title] Therapy-related changes of CD20+ and CD45RO+ lymphocyte subsets in chronic myeloid leukemia (CML): an immunohistochemical and morphometric study on sequential trephine biopsies of the bone marrow.
  • Little information exists about the amount of CD45RO+-T- and CD20+-B-lymphocytes in the bone marrow of patients with Philadelphia chromosome-positive chronic myelogenous leukemia (Ph1+-CML) at presentation or regarding corresponding changes during therapy.
  • Therefore, an immunohistological and morphometric study was performed on 219 representative trephine biopsies of the bone marrow derived from 70 patients with repeated examinations during the course of Ph1+-CML.
  • In comparison to a control group and calculated per hematopoietic cells, the CML bone marrow showed about a 50% decrease in the total amount of lymphocytes.
  • Determination of CD45RO+ and CD20+ subsets revealed a significant enhancement during treatment.
  • Because of the different intervals (range, 10 to 25 mo) between first and last biopsy in the various therapeutic groups, results had to be modified by considering dynamic features.
  • This calculation included changes of the lymphocyte subpopulations related to time.
  • Contrasting the CD45RO+ lymphocytes, a relevant increase in the CD20+ subset could be observed after interferon-a treatment or corresponding combination regimens.
  • No significant correlations were found between fiber density at onset (first biopsy) or development of fibrosis and lymphocyte proliferations in the course of CML.
  • Our results are in keeping with the finding that a proper immune response consistent with an increased lymphocyte growth seems to be associated with a regression of the clonally-transformed cell population.
  • [MeSH-major] Antigens, CD20 / immunology. Antigens, CD45 / immunology. Antineoplastic Agents / therapeutic use. Bone Marrow / immunology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Lymphocyte Subsets / immunology
  • [MeSH-minor] Adult. Biopsy. Busulfan / therapeutic use. Cohort Studies. Drug Therapy, Combination. Female. Humans. Hydroxyurea / therapeutic use. Immunoenzyme Techniques. Interferon-alpha / therapeutic use. Male. Middle Aged. Vincristine / therapeutic use

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  • (PMID = 10955456.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antineoplastic Agents; 0 / Interferon-alpha; 5J49Q6B70F / Vincristine; EC 3.1.3.48 / Antigens, CD45; G1LN9045DK / Busulfan; X6Q56QN5QC / Hydroxyurea
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5. Myojo T, Hino N: Complete remission from chronic myelogenous leukemia--blastic crisis caused by reduced intensity stem cell transplantation following partial remission due to imatinib. Intern Med; 2004 Feb;43(2):126-30
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  • [Title] Complete remission from chronic myelogenous leukemia--blastic crisis caused by reduced intensity stem cell transplantation following partial remission due to imatinib.
  • We report a 55-year-old man who showed no change after chemotherapy for chronic myelogenous leukemia-blastic crisis (CML-BC) in 1998.
  • Allo-peripheral blood stem cell transplantation (PBSCT) was then performed and Complete remission (CR) was achieved, but recurrence was seen in 2001.
  • The bcr-abl gene disappeared and Ph1 chromosome disappearance was ascertained.
  • CR was thus achieved.
  • There are still no established radical methods of treating CML-BC.
  • Thus, therapy by allograft after the patient has entered hematological remission with imatinib is considered a new way of dealing with cases of CML-BC.
  • [MeSH-major] Blast Crisis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Peripheral Blood Stem Cell Transplantation / methods. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Bone Marrow / pathology. Genes, abl. Humans. Hyperplasia. Imatinib Mesylate. Male. Middle Aged. Philadelphia Chromosome. Translocation, Genetic

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  • (PMID = 15005255.001).
  • [ISSN] 0918-2918
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
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6. Uno K, Inukai T, Kayagaki N, Goi K, Sato H, Nemoto A, Takahashi K, Kagami K, Yamaguchi N, Yagita H, Okumura K, Koyama-Okazaki T, Suzuki T, Sugita K, Nakazawa S: TNF-related apoptosis-inducing ligand (TRAIL) frequently induces apoptosis in Philadelphia chromosome-positive leukemia cells. Blood; 2003 May 1;101(9):3658-67
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  • [Title] TNF-related apoptosis-inducing ligand (TRAIL) frequently induces apoptosis in Philadelphia chromosome-positive leukemia cells.
  • Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and Fas ligand (FasL) have been implicated in antitumor immunity and therapy.
  • In the present study, we investigated the sensitivity of Philadelphia chromosome (Ph1)-positive leukemia cell lines to TRAIL- or FasL-induced cell death to explore the possible contribution of these molecules to immunotherapy against Ph1-positive leukemias.
  • TRAIL, but not FasL, effectively induced apoptotic cell death in most of 5 chronic myelogenous leukemia-derived and 7 acute leukemia-derived Ph1-positive cell lines.
  • Moreover, primary leukemia cells from Ph1-positive acute lymphoblastic leukemia patients were also sensitive to TRAIL, but not to FasL, depending on DR4/DR5 expression.
  • Fas-associated death domain protein (FADD) and caspase-8, components of death-inducing signaling complex (DISC), as well as FLIP (FLICE [Fas-associating protein with death domain-like interleukin-1-converting enzyme]/caspase-8 inhibitory protein), a negative regulator of caspase-8, were expressed ubiquitously in Ph1-positive leukemia cell lines irrespective of their differential sensitivities to TRAIL and FasL.
  • Notably, TRAIL could induce cell death in the Ph1-positive leukemia cell lines that were refractory to a BCR-ABL-specific tyrosine kinase inhibitor imatinib mesylate (STI571; Novartis Pharma, Basel, Switzerland).
  • These results suggested the potential utility of recombinant TRAIL as a novel therapeutic agent and the possible contribution of endogenously expressed TRAIL to immunotherapy against Ph1-positive leukemias.
  • [MeSH-major] Apoptosis / drug effects. Arabidopsis Proteins. Intracellular Signaling Peptides and Proteins. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Membrane Glycoproteins / pharmacology. Neoplastic Stem Cells / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Amino Acid Chloromethyl Ketones / pharmacology. Apoptosis Regulatory Proteins. Benzamides. CASP8 and FADD-Like Apoptosis Regulating Protein. Carrier Proteins / physiology. Caspase 1 / physiology. Death Domain Receptor Signaling Adaptor Proteins. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor. Enzyme Inhibitors / pharmacology. Fas Ligand Protein. Fatty Acid Desaturases / physiology. Fusion Proteins, bcr-abl / antagonists & inhibitors. Humans. Imatinib Mesylate. Leupeptins / pharmacology. NF-kappa B / antagonists & inhibitors. Neoplasm Proteins / antagonists & inhibitors. Neoplasm Proteins / physiology. Peptides / pharmacology. Piperazines / pharmacology. Pyrimidines / pharmacology. Receptors, TNF-Related Apoptosis-Inducing Ligand. Receptors, Tumor Necrosis Factor / physiology. Recombinant Proteins / pharmacology. TNF-Related Apoptosis-Inducing Ligand. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / pathology

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  • (PMID = 12506034.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acid Chloromethyl Ketones; 0 / Apoptosis Regulatory Proteins; 0 / Arabidopsis Proteins; 0 / Benzamides; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CFLAR protein, human; 0 / Carrier Proteins; 0 / Death Domain Receptor Signaling Adaptor Proteins; 0 / Enzyme Inhibitors; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Intracellular Signaling Peptides and Proteins; 0 / Leupeptins; 0 / Membrane Glycoproteins; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Peptides; 0 / Piperazines; 0 / Pyrimidines; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Recombinant Proteins; 0 / SN50 peptide; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 0 / TNFRSF10B protein, human; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 110044-82-1 / acetylleucyl-leucyl-norleucinal; 8A1O1M485B / Imatinib Mesylate; EC 1.14.19.- / Fatty Acid Desaturases; EC 1.14.99.- / Fad7 protein, Arabidopsis; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.4.22.36 / Caspase 1
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