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Your search keyword '"Gjertsen, B."' showing total 21 results
Start Over Author "Gjertsen, B." Journal leukemia
21 results on '"Gjertsen, B."'

3. Correction: Lenalidomide added to standard intensive treatment for older patients with AML and high-risk MDS

Author

Ossenkoppele, G. J., Breems, D. A., Stuessi, G., van Norden, Y., Bargetzi, M., Biemond, B. J., A von dem Borne, P., Chalandon, Y., Cloos, J., Deeren, D., Fehr, M., Gjertsen, B., Graux, C., Huls, G., Janssen, J. J. J. W., Jaspers, A., Jongen-Lavrencic, M., de Jongh, E., Klein, S. K., van der Klift, M., van Marwijk Kooy, M., Maertens, J., Michaux, L., van der Poel, M. W. M., van Rhenen, A., Tick, L., Valk, P., Vekemans, M. C., van der Velden, W. J. F. M., de Weerdt, O., Pabst, T., Manz, M., and Löwenberg, B.

Published
2020
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5. Lenalidomide added to standard intensive treatment for older patients with AML and high-risk MDS

Author

Ossenkoppele, G.J., Breems, D.A., Stuessi, G., Norden, Y. van, Bargetzi, M., Biemond, B.J., Borne, P.A. von dem, Chalandon, Y., Cloos, J., Deeren, D., Fehr, M., Gjertsen, B., Graux, C., Huls, G., Janssen, J.J.J.W., Jaspers, A., Jongen-Lavrencic, M., Jongh, E. de, Klein, S.K., Klift, M. van der, Kooy, M.V., Maertens, J., Micheaux, L., Poel, M.W.M. van der, Rhenen, A. van, Tick, L., Valk, P., Vekemans, M.C., Velden, W.J.F.M. van der, Weerdt, O. de, Pabst, T., Manz, M., Lowenberg, B., Havelange, Moors, I., Obberg, F. van, Maertens, J.A., Hodossy, B., Vansteenweghen, S., Lammertijn, L., Sonet, A., Triffet, A., Gjertsen, B.T., Passweg, J., Heim, D., Giovanni, S., Betticher, D., Spertini, O., Gregor, M., Hess, U., Manz, M.G., Loosdrecht, A. van de, Janssen, J.J.W.M., Esser, J.W.J. van, Brouwer, R.E., Lammeren-Venema, D. van, Levin, M.D., Tick, L.W., Legdeur, M.C.J.C., Vellenga, E., Hoogendoorn, M., Veelken, J.H., Schouten, H.C., Cornelissen, J., Wouters, B., Raaijmakers, H.G.M., Kuball, J., Dutch-Belgian Hemato-Oncology, Swiss Grp Clinical Canc Res SAKK, Stem Cell Aging Leukemia and Lymphoma (SALL), Guided Treatment in Optimal Selected Cancer Patients (GUTS), Clinical Haematology, CCA - Cancer Treatment and Quality of Life, CCA - Cancer Treatment and quality of life, Hematology laboratory, Hematology, Department of History, International Institute of Social Studies, RS: GROW - R3 - Innovative Cancer Diagnostics & Therapy, Interne Geneeskunde, MUMC+: MA Hematologie (9), UCL - SSS/DDUV - Institut de Duve, UCL - SSS/DDUV/MEXP - Médecine expérimentale, UCL - SSS/IREC/MONT - Pôle Mont Godinne, UCL - SSS/IREC/SLUC - Pôle St.-Luc, UCL - (MGD) Service d'hématologie, and UCL - (SLuc) Service d'hématologie

Subjects
0301 basic medicine, Cancer Research, medicine.medical_specialty, medicine.medical_treatment, Phases of clinical research, HIGH-DOSE LENALIDOMIDE, ACUTE MYELOID-LEUKEMIA, THERAPY, 03 medical and health sciences, 0302 clinical medicine, Older patients, SDG 3 - Good Health and Well-being, Internal medicine, medicine, 610 Medicine & health, Adverse effect, Lenalidomide, Chemotherapy, business.industry, Intensive treatment, Myeloid leukemia, Hematology, ADULTS, 030104 developmental biology, Oncology, 030220 oncology & carcinogenesis, Inflammatory diseases Radboud Institute for Health Sciences [Radboudumc 5], Cytarabine, business, medicine.drug
Abstract

Contains fulltext : 225470.pdf (Publisher’s version ) (Closed access) More effective treatment modalities are urgently needed in patients with acute myeloid leukemia (AML) of older age. We hypothesized that adding lenalidomide to intensive standard chemotherapy might improve their outcome. After establishing a safe lenalidomide, dose elderly patients with AML were randomly assigned in this randomized Phase 2 study (n = 222) to receive standard chemotherapy ("3 + 7") with or without lenalidomide at a dose of 20 mg/day 1-21. In the second cycle, patients received cytarabine 1000 mg/m(2) twice daily on days 1-6 with or without lenalidomide (20 mg/day 1-21). The CR/CRi rates in the two arms were not different (69 vs. 66%). Event-free survival (EFS) at 36 months was 19% for the standard arm versus 21% for the lenalidomide arm and overall survival (OS) 35% vs. 30%, respectively. The frequencies and grade of adverse events were not significantly different between the treatment arms. Cardiovascular toxicities were rare and equally distributed between the arms. The results of the present study show that the addition of lenalidomide to standard remission induction chemotherapy does not improve the therapeutic outcome of older AML patients. This trial is registered as number NTR2294 in The NederlandsTrial Register (www.trialregister.nl).

Published
2020
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14. HOX gene expression predicts response to BCL-2 inhibition in acute myeloid leukemia

Author

Kontro, M, primary, Kumar, A, additional, Majumder, M M, additional, Eldfors, S, additional, Parsons, A, additional, Pemovska, T, additional, Saarela, J, additional, Yadav, B, additional, Malani, D, additional, Fløisand, Y, additional, Höglund, M, additional, Remes, K, additional, Gjertsen, B T, additional, Kallioniemi, O, additional, Wennerberg, K, additional, Heckman, C A, additional, and Porkka, K, additional

Published
2016
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16. HOXgene expression predicts response to BCL-2 inhibition in acute myeloid leukemia

Author

Kontro, M, Kumar, A, Majumder, M M, Eldfors, S, Parsons, A, Pemovska, T, Saarela, J, Yadav, B, Malani, D, Fløisand, Y, Höglund, M, Remes, K, Gjertsen, B T, Kallioniemi, O, Wennerberg, K, Heckman, C A, and Porkka, K

Abstract

Inhibitors of B-cell lymphoma-2 (BCL-2) such as venetoclax (ABT-199) and navitoclax (ABT-263) are clinically explored in several cancer types, including acute myeloid leukemia (AML), to selectively induce apoptosis in cancer cells. To identify robust biomarkers for BCL-2 inhibitor sensitivity, we evaluated the ex vivosensitivity of fresh leukemic cells from 73 diagnosed and relapsed/refractory AML patients, and then comprehensively assessed whether the responses correlated to specific mutations or gene expression signatures. Compared with samples from healthy donor controls (nonsensitive) and chronic lymphocytic leukemia (CLL) patients (highly sensitive), AML samples exhibited variable responses to BCL-2 inhibition. Strongest CLL-like responses were observed in 15% of the AML patient samples, whereas 32% were resistant, and the remaining exhibited intermediate responses to venetoclax. BCL-2 inhibitor sensitivity was associated with genetic aberrations in chromatin modifiers, WT1and IDH1/IDH2. A striking selective overexpression of specific HOXAand HOXBgene transcripts were detected in highly BCL-2 inhibitor sensitive samples. Ex vivoresponses to venetoclax showed significant inverse correlation to β2-microglobulin expression and to a lesser degree to BCL-XLand BAXexpression. As new therapy options for AML are urgently needed, the specific HOXgene expression pattern can potentially be used as a biomarker to identify venetoclax-sensitive AML patients for clinical trials.

Published
2017
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19. Safety and efficacy of the combination of pegylated interferon-a2b and dasatinib in newly diagnosed chronic-phase chronic myeloid leukemia patients

Author

Hjorth-Hansen, H, Stentoft, J, Richter, J, Koskenvesa, P, Höglund, M, Dreimane, A, Porkka, K, Gedde-Dahl, T, Gjertsen, B T, Gruber, F X, Stenke, L, Eriksson, K M, Markevärn, B, Lübking, A, Vestergaard, H, Udby, L, Bjerrum, O W, Persson, I, Mustjoki, S, and Olsson-Strömberg, U

Abstract

Dasatinib (DAS) and interferon-a have antileukemic and immunostimulatory effects and induce deep responses in chronic myeloid leukemia (CML). We assigned 40 newly diagnosed chronic-phase CML patients to receive DAS 100?mg o.d. followed by addition of pegylated interferon-a2b (PegIFN) after 3 months (M3). The starting dose of PegIFN was 15?µg/week and it increased to 25?µg/week at M6 until M15. The combination was well tolerated with manageable toxicity. Of the patients, 84% remained on PegIFN at M12 and 91% (DAS) and 73% (PegIFN) of assigned dose was given. Only one patient had a pleural effusion during first year, and three more during the second year. After introduction of PegIFN we observed a steep increase in response rates. Major molecular response was achieved in 10%, 57%, 84% and 89% of patients at M3, M6, M12 and M18, respectively. At M12, MR4was achieved by 46% and MR4.5by 27% of patients. No patients progressed to advanced phase. In conclusion, the combination treatment appeared safe with very promising efficacy. A randomized comparison of DAS±PegIFN is warranted.

Published
2016
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20. Animal models of acute myelogenous leukaemia - development, application and future perspectives.

Author

McCormack E, Bruserud O, and Gjertsen BT

Subjects
Animals, Genetic Engineering, Humans, Neoplasm Transplantation, Xenograft Model Antitumor Assays, Disease Models, Animal, Leukemia, Myeloid, Acute genetics, Leukemia, Myeloid, Acute pathology, Leukemia, Myeloid, Acute therapy
Abstract

From the early inception of the transplant models through to contemporary genetic and xenograft models, evolution of murine leukaemic model systems have been critical to our general comprehension and treatment of cancer, and, more specifically, disease states such as acute myelogenous leukaemia (AML). However, even with modern advances in therapeutics and molecular diagnostics, the majority of AML patients die from their disease. Thus, in the absence of definitive in vitro models which precisely recapitulate the in vivo setting of human AMLs and failure of significant numbers of new drugs late in clinical trials, it is essential that murine AML models are developed to exploit more specific, targeted therapeutics. While various model systems are described and discussed in the literature from initial transplant models such as BNML and spontaneous murine leukaemia virus models, to the more definitive genetic and clinically significant NOD/SCID xenograft models, there exists no single compendium which directly assesses, reviews or compares the relevance of these models. Thus, the function of this article is to provide clinicians and experimentalists a chronological, comprehensive appraisal of all AML model systems, critical discussion on the elucidation of their roles in our understanding of AML and consideration to their efficacy in the development of AML chemotherapeutics.

Published
2005
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21. Effects of interleukin 10 on blast cells derived from patients with acute myelogenous leukemia.

Author

Bruserud O, Tore Gjertsen B, Brustugun OT, Bassøe CF, Nesthus I, Espen Akselsen P, Bühring HJ, and Pawelec G

Subjects
Aged, Apoptosis drug effects, Blast Crisis pathology, Cell Differentiation drug effects, Cell Division drug effects, Female, Humans, Immunophenotyping, Lymphocyte Activation drug effects, Male, Middle Aged, Tumor Cells, Cultured, Cytokines metabolism, Interleukin-10 pharmacology, Leukemia, Myeloid, Acute pathology
Abstract

The effect of interleukin 10 (IL-10) on proliferation and cytokine secretion by acute myelogenous leukemia (AML) blast cells was investigated in vitro. IL-10 inhibited spontaneous AML blast proliferation for a majority of patients, whereas in the presence of exogenous growth factors (granulocyte-stimulating factor, G-CSF; granulocyte-macrophage colony-stimulating factor, GM-CSF; interleukin 3) the IL-10 effect on blast proliferation showed a wide variation depending on the individual AML patient. IL-10 seemed to cause an irreversible inhibitory effect on AML blasts, as inhibition could also be demonstrated when IL-10 was present only during the initial preincubation of the leukemia cells. IL-10 also inhibited AML blast colony formation. However, independent of the effect on AML blast proliferation, IL-10 decrease cytokine secretion from AML blast cells for all patients, as demonstrated for IL-1 alpha, IL-1 beta, tumor necrosis factor-alpha, GM-CSF and interleukin 6. IL-10 did not inhibit development of apoptosis in AML blasts cultured in vitro. Expression of complement receptors and capability to adhere and internalize bacteria by AML blasts were not altered by IL-10.

Published
1995

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