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  • 1
    Keywords: EXPRESSION ; Germany ; QUANTIFICATION ; TIME ; PATIENT ; treatment ; ALPHA ; ASSAY ; DECREASE ; POLYMERASE-CHAIN-REACTION ; INTERFERON
    Abstract: We developed a real-time quantitative polymerase chain reaction-based assay for quantification of PRV-1 mRNA. We found that the expression of PRV-1 in granulocytes of patients with polycythemia vera (PV) who were pretreated with phlebotomy or hydroxyurea was significantly higher than that in normal controls. Surprisingly, in PV patients who had received interferon-alpha (IFN) for five or more months no significant PRV-1 upregulation was found. Observation of four PV patients treated with IFN over six months revealed a uniform time- dependent decrease of initially upregulated PRV-1
    Type of Publication: Journal article published
    PubMed ID: 12651277
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  • 2
    Keywords: CANCER ; CELLS ; tumor ; BLOOD ; CELL ; Germany ; THERAPY ; TIME ; PATIENT ; TRANSPLANTATION ; treatment ; BONE-MARROW ; BREAST-CANCER ; TARGET ; chemotherapy ; EFFICIENT ; STEM-CELLS ; PROGENITOR CELLS ; CANCER-PATIENTS ; BODY ; CYCLOPHOSPHAMIDE ; CANCER PATIENTS ; PERIPHERAL-BLOOD ; MULTICENTER ; MULTIPLE-MYELOMA ; SINGLE ; HIGH-DOSE CHEMOTHERAPY ; multiple myeloma ; ONCOLOGY ; WEIGHT ; stem cells ; dexamethasone ; pegfilgrastim ; MOBILIZATION ; immunology ; STEM ; myeloma ; ADJUNCT ; ADMINISTRATION PEGFILGRASTIM ; apheresis ; DAILY FILGRASTIM ; peripheral blood stem cell ; PRETREATED LYMPHOMA PATIENTS ; REGIMEN ; STAGE-II
    Abstract: High-dose chemotherapy followed by autologous blood stem cell transplantation is the standard treatment for myeloma patients. In this study, CAD (cyclophosphamide, adriamycin, dexamethasone) chemotherapy and a single dose of peg. lgrastim (12 mg) was highly effective ve in mobilizing peripheral blood stem cells (PBSCs) for subsequent transplantation, with 88% of patients (n = 26) achieving the CD34(+) cell harvest target of 〉= 7.50 x 106 CD34(+) cells/ kg body weig ht, following a median of two apheresis procedures (range 1 -4) and with. rst apheresis performed at a median day 13 after CAD application (range 10 -20). Patients treated with peg. lgrastim showed a reduced time to. rst apheresis procedure from mobilization compared with. lgrastim-mobilized historical matched controls (n = 52, P = 0.015). The peg. lgrastim mobilization regimen allowed for transplantation of a median of 3.58 x 10 6 CD34(+) cells/ kg body weight while leaving suf. ficient stored cells for a second high-dose regimen and back-ups in most patients. Engraftment following transplantation was comparable to. lgrastim, with a median time of 14 days to leucocyte 〉= 1.0 x 109/l (range 10 -21) and 11 days to platelets 〉= 20 x 109/l (range 0 -15). The results of this study thus provide further support for the clinical utility of peg. lgrastim for the mobilization of PBSC following chemotherapy in cancer patients scheduled for transplantation
    Type of Publication: Journal article published
    PubMed ID: 17450182
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  • 3
    Keywords: CELLS ; CELL ; Germany ; human ; THERAPY ; CLASSIFICATION ; SITE ; GENE ; GENOME ; TISSUE ; gene therapy ; MICE ; DNA ; TISSUES ; MR ; BONE-MARROW ; NOD/Scid mice ; ACID ; NUCLEIC-ACIDS ; IMMUNODEFICIENT MICE ; STEM-CELLS ; POLYMERASE-CHAIN-REACTION ; CD34(+) CELLS ; PERIPHERAL-BLOOD ; GENE-THERAPY ; HEMATOPOIETIC STEM-CELLS ; IMMUNE-DEFICIENT MICE ; clonality ; JUNCTIONS ; LIBRARIES ; BLOOD PROGENITOR CELLS ; experimental PBPC transplantation ; RESISTANCE 1 GENE ; SCID-repopulating cells ; single cell analysis ; TIME QUANTITATIVE PCR
    Abstract: Methods to analyze the clonality of an adverse event in preclinical or clinical retroviral stem cell gene therapy protocols are needed. We analyzed the progeny of retrovirally transduced human peripheral blood progenitor cells (PBPCs) after transplantation and engraftment in immune-deficient mice. The integration site of the provirus serves as a unique tag of the individual transduced PBPC. A plasmid library of junctions between proviral and human genomic DNA was generated. We were able to detect individual transduced cell clones that amounted to 0.14%-0.0001% of chimeric bone marrow cells. This is the first report in which the contribution of individual marrow-repopulating cells to human hematopoiesis is directly quantified
    Type of Publication: Journal article published
    PubMed ID: 15277702
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  • 4
    Keywords: APOPTOSIS ; CELLS ; IN-VITRO ; INHIBITOR ; COMBINATION ; Germany ; INHIBITION ; THERAPY ; TYROSINE KINASE ; PROTEIN ; LINES ; MECHANISM ; mechanisms ; CELL-LINES ; resistance ; LINE ; OVEREXPRESSION ; CHRONIC MYELOGENOUS LEUKEMIA ; CHRONIC MYELOID-LEUKEMIA ; imatinib ; drug resistance ; DRUG-RESISTANCE ; cell lines ; MESYLATE ; P-GLYCOPROTEIN ; CHEMOTHERAPEUTIC DRUGS ; PLUS ; MDR1 ; BCR-ABL ; PHILADELPHIA-CHROMOSOME ; PGP ; 17-AAG ; CHROMOSOME-POSITIVE LEUKEMIA ; CLINICAL RESISTANCE ; STI571 ; synergism
    Abstract: Overexpression of BCR-ABL and P-glycoprotein (Pgp) are two of the known mechanisms of imatinib resistance. As combination therapy may allow to overcome drug resistance, we investigated the effect of combination treatment with imatinib and 17-allylamino-17-demethoxygeldanamycin (17-AAG), a heat-shock protein 90 (Hsp90) inhibitor, on different imatinib-Sensitive and imatinib-resistant CML cell lines. In imatinib-sensitive cells, combination index (CI) values obtained using the method of Chou and Talalay indicated additive ( CI 1) or marginally antagonistic (CI 〉 1) effects following simultaneous treatment with imatinib and 17-AAG. In imatinib-resistant cells both drugs acted synergistically (CI 〈 1). In primary chronic-phase CML cells additive or synergistic effects of the combination of imatinib plus 17-AAG were discernible. Annexin V/propidium iodide staining showed that the activity of imatinib plus 17-AAG is mediated by apoptosis. Combination treatment with imatinib plus 17-AAG was more effective in reducing the BCR-ABL protein level than 17-AAG alone. Monotherapy with 17-AAG decreased P-glycoprotein activity, which may increase intracellular imatinib levels and contribute to the sensitization of CML cells to imatinib. The results suggest that combination of imatinib and 17-AAG may be useful to overcome imatinib resistance in a clinical setting
    Type of Publication: Journal article published
    PubMed ID: 15902298
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  • 5
    Keywords: CELLS ; EXPRESSION ; INHIBITOR ; BLOOD ; CELL ; Germany ; KINASE ; PATHWAY ; TYROSINE KINASE ; RNA ; transcription ; cell line ; LINES ; PATIENT ; MECHANISM ; FLOW ; CELL-LINES ; TYROSINE KINASE INHIBITOR ; MOLECULE ; bone marrow ; BONE-MARROW ; leukemia ; LINE ; TRAFFICKING ; ADHESION ; CELL-ADHESION ; PROGENITOR CELLS ; POLYMERASE-CHAIN-REACTION ; ADHESION MOLECULE ; CD34(+) CELLS ; CHRONIC MYELOGENOUS LEUKEMIA ; chronic myelogenous leukemia,adhesion molecule,L-selectin,imatinib mesylate ; CHRONIC MYELOID-LEUKEMIA ; CYTOGENETIC RESPONSES ; FLOW-CYTOMETRY ; HEMATOPOIETIC PROGENITOR CELLS ; HEMATOPOIETIC-CELLS ; imatinib ; INTERFERON-ALPHA RESTORES ; L-SELECTIN EXPRESSION ; MARROW STROMA ; PERIPHERAL-BLOOD
    Abstract: Chronic myelogenous leukemia (CML) is characterized by aberrant trafficking of malignant hematopoietic progenitor cells in the peripheral blood. Expression of the cell adhesion molecule CD62L was reported to be significantly lower in CML patients than in normal controls. We studied whether the transcription of CD62L in CML cells is dependent on the activity of the BCR-ABL tyrosine kinase. Following addition of the Abelson (ABL) tyrosine kinase inhibitor imatinib (formerly STI571) to two BCR-ABL-positive cell lines (BV173, SD-1), we observed a dose-dependent increase in CD62L RNA levels of up to 45-fold by a quantitative, real-time polymerase chain reaction and an increase in the amount of cell surface-bound CD62L of up to 18-fold by quantitative flow cytometry, respectively. These data are validated by an increased CD62L expression in the bone marrow of patients (n=6) with advanced CML who received imatinib. Restoration of defective cell adhesion mediated via the CD62L pathway may be one mechanism of action of imatinib in BCR-ABL-positive leukemias
    Type of Publication: Journal article published
    PubMed ID: 12714574
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  • 6
    Keywords: APOPTOSIS ; CELLS ; GROWTH ; AGENTS ; Germany ; INHIBITION ; THERAPY ; TYROSINE KINASE ; DEATH ; LINES ; PATIENT ; CELL-LINES ; treatment ; STAGE ; ASSAY ; resistance ; CELL-DEATH ; CELL-LINE ; leukemia ; LINE ; ACUTE LYMPHOBLASTIC-LEUKEMIA ; CHRONIC MYELOGENOUS LEUKEMIA ; CHRONIC MYELOID-LEUKEMIA ; imatinib ; cell lines ; HEMATOLOGIC MALIGNANCIES ; INHIBITORS ; P-GLYCOPROTEIN ; ASSAYS ; PHASE ; BCR-ABL ; CML ; PHILADELPHIA-CHROMOSOME ; RESISTANT ; MONOTHERAPY ; FARNESYL TRANSFERASE INHIBITOR ; farnesyltransferase inhibitor ; L744,832 ; LB42918 ; LOW-DOSE CYTARABINE ; RAS SIGNALING PATHWAY
    Abstract: 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. Materials and Methods: Growth inhibition of the cell lines and primary patient cells was assessed by MTT assays and colony-forming cell assays, respectively. Drug interactions were analyzed according to the median-effect method of Chou and Talalay. The determination of apoptotic cell death was performed by annexin V/propidium iodide staining. Results: Combinations of both FTIs with imatinib displayed synergism or sensitization (potentiation) in all the cell lines tested. 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
    Type of Publication: Journal article published
    PubMed ID: 16827161
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