22 research outputs found

    Current Concepts and Newer Developments in the Treatment of Malignant Gliomas

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    Primary malignant brain tumors account for only 2% of all adult cancers but they cause a disproportionately high cancer-related disability and death. Survival of malignant glioma patients has changed only modestly over the past three decades despite the emergence of new treatment strategies for these tumors. In this review, we describe the standard treatment modalities for malignant glioma, which include surgery, radiation therapy and chemotherapy, as well as the status of novel therapies that have been developed to target various aspects of glioma cell biology. We also address this issue of drug delivery as a factor limiting the efficacy of systemic administration of therapeutics and attempts to overcome this barrier. Further progress towards a cure for malignant gliomas will require a greater understanding of the underlying mechanisms driving the growth, and resistance to therapy, of these challenging tumors

    Current Concepts and Newer Developments in the Treatment of Malignant Gliomas

    No full text
    Primary malignant brain tumors account for only 2% of all adult cancers but they cause a disproportionately high cancer-related disability and death. Survival of malignant glioma patients has changed only modestly over the past three decades despite the emergence of new treatment strategies for these tumors. In this review, we describe the standard treatment modalities for malignant glioma, which include surgery, radiation therapy and chemotherapy, as well as the status of novel therapies that have been developed to target various aspects of glioma cell biology. We also address this issue of drug delivery as a factor limiting the efficacy of systemic administration of therapeutics and attempts to overcome this barrier. Further progress towards a cure for malignant gliomas will require a greater understanding of the underlying mechanisms driving the growth, and resistance to therapy, of these challenging tumors

    Ida-FLAG chemotherapy in the refractory-relapsed hematologic malignancies [Refrakter-relapsli hematolojik maligniteli olgularda Ida-FLAG kemoterapisi]

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    Ida-FLAG chemotherapy, which consists of fludarabine, high dose cytosine arabinoside, idarubucine, and G-CSF, is accepted as an efficient chemotherapeutical regimen in the refractory and/or relapsed AML, ALL, and relapsed malign lymphomas. In this report, the result of the patients who have recieved Ida-FLAG regimen in our center, have been evaluated retrospectively. Total 10 patients were included and mean age was 41.1±11.2 years. Seven of them were relapsed or refractory AML, 2 of them relapsed ALL and one patient was transformed low grade lymphoma. All of the patients had recieved multiple chemotherapy regimens before. All patients died bacaues of febrile neutropenia, hemorrhage and bone marrow failure. In the literature, Ida-FLAG results are better and the mortality is less. In our patients, the mortality was high, most probably because of very bad prognosis patient selection. With our results, it can be suggested that, Ida-FLAG is not a good choice in the selected patient group of relapsed-refractory, multiple chemotherapy administered patients

    Augmentation of methylprednisolone-induced differentiation of myeloid leukemia cells by serine/threonine protein phosphatase inhibitors

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    PubMed ID: 10374865To elucidate the roles of serine/threonine protein phosphatases type 1 (PP1) and type 2A (PP2A) in methylprednisolone-induced differentiation of HL60 cells into granulocytes and K562 cells into monocytes, we examined the effect of serine/threonine protein phosphatase inhibitors, okadaic acid and Cal-A on the proliferation/differentiation of HL60 and K562 cells. Okadaic acid and Cal-A augmented methylprednisolone induced granulocytic differentiation and cell death of HL60 cells and monocytic differentiation and cell death of K562 cells in different dose ranges, respectively. These data suggest an important role of PP1 and PP2A in the mechanism leading to differentiation of leukemic cells
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