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Showing result 1 - 5 of 194 swedish dissertations matching the above criteria.
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1. Targeting residual malignant cells in myeloid leukemia
Abstract : Malignant cells persisting during treatment prevent cure in many patients with myeloid leukemia. In acute myeloid leukemia (AML), the failure to eradicate the leukemic clone during conventional chemotherapy is associated with leukemic relapse, mostly with dismal survival outcome. READ MORE
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2. Immunotherapy and immunosuppression in myeloid leukemia
Abstract : Acute myeloid leukemia (AML) and chronic myelomonocytic leukemia (CMML) are potentially life-threatening blood cancers characterized by the expansion of malignant myeloid cells in bone marrow and other organs. This thesis aimed at contributing to the understanding of the role of natural killer (NK) cells in AML and CMML with focus on the potential impact of the immunosuppression exerted by reactive oxygen species (ROS) formed by the myeloid cell NOX2 enzyme. READ MORE
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3. Chronic myeloid leukemia and cancer
Abstract : Background Chronic myeloid leukemia (CML) is a relatively rare hematological malignancy with a constant incidence of approximately 90 new cases each year in Sweden (0.9 cases/100 000 inhabitants). The etiology is largely unknown but high doses of ionizing radiation are a known but rare risk factor. READ MORE
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4. Perinatal Risk Factors for Childhood Leukemia
Abstract : The aim of the studies described in this thesis was to assess the association between certain perinatal factors and the risk of childhood lymphatic and myeloid leukemia and infant leukemia. The five studies presented were all conducted in Sweden as population-based case-control studies. READ MORE
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5. Functional Modeling of Genes Upregulated in Chronic Myeloid Leukemia
Abstract : Chronic myeloid leukemia (CML) is caused by the transformation of a primitive hematopoietic cell by the BCR/ABL1 fusion gene that is formed through the chromosomal translocation t(9;22). CML is currently successfully treated with tyrosine kinase inhibitors targeting the ABL1 kinase domain. READ MORE