The Experts below are selected from a list of 9 Experts worldwide ranked by ideXlab platform
Michał Maurin - One of the best experts on this subject based on the ideXlab platform.
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Antitumor activity of platinum(II) complexes with histamine and radioiodinated histamine in a transplantable murine adenocarcinoma model
Nuclear medicine and biology, 2008Co-Authors: Piotr Garnuszek, Urszula Karczmarczyk, Michał MaurinAbstract:Abstract Purpose Antitumor activity of the dichloroplatinum(II)–histamine complexes labeled with I-125 or I-131 was investigated in a transplantable murine adenocarcinoma (MA) model. Methods The tumor model was obtained in C3H/W female mice after subcutaneous inoculation of the tumor cells derived from the mice bearing a mammary tumor of spontaneous origin. Antitumor activities of the platinum-histamine complexes were investigated in three independent experiments, which differed in applied doses of preparations (PtCl 2 Hist, PtCl 2 [ 125 I]Hist, PtCl 2 [ 131 I]Hist, PtCl 2 Hist/PtCl 2 [ 125 I]Hist and PtCl 2 Hist/PtCl 2 [ 131 I]Hist), treatment schedules as well as stages of the disease progress in the animals used. Experiment 1 included long-term, multidose treatment with low single doses (treatment duration 31–32 days; 8–10 doses of ca. 0.25∙MTD Pt each). Experiment 2 included short-term, multidose treatment with higher single doses (4×ca. 0.5∙MTD Pt up to Day 13 of the treatment). Experiment 3 included long-term concomitant multidose treatment with higher single doses (9×0.9–0.4∙MTD Pt up to Day 33). Results The long-term treatment with the platinum-histamine preparations revealed inhibiting activity on the tumor growth and size in comparison to control groups. The most intensive and significant antitumor effects were observed for the radioactive complexes. The tumor growth delay factors (GDFs) observed in Experiment 1 were 0.4, 0.7, and 1.2 for PtCl 2 Hist, PtCl 2 Hist/PtCl 2 [ 131 I]Hist, and PtCl 2 Hist/PtCl 2 [ 125 I]Hist, respectively. Significant ( P .05 ) prolongations of median survivals (MS) were found in Experiment 2 following the treatment with higher single doses of PtCl 2 Hist and PtCl 2 His/PtCl 2 [ 125 I]Hist (Ratio MS tr /MS con ca. 1.4). A slightly less potent activity was observed for PtCl 2 Hist/PtCl 2 [ 131 I]Hist, and no survival improvement was found for the groups treated mostly with the radiation (PtCl 2 [ 125 I]Hist and PtCl 2 [ 131 I]Hist). The intensive and long-term concomitant scheduling of the radioactive platinum–histamine complexes labeled with I-125 and I-131 (Experiment 3) resulted in a significant inhibition of the tumor growth (GDF=1.9) and survival prolongation of the tumor-bearing mice (MS tr /MS con =1.5, P =.023). The treatment-related toxicity was mild. Conclusion An enhancement of the antitumor activity due to the multidose concomitant treatment with a combination of cytotoxic/cytostatic dichloroplatinum(II)–histamine and the attached iodine radionuclides was shown in the murine model of Experimental Neoplasm.
Piotr Garnuszek - One of the best experts on this subject based on the ideXlab platform.
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Antitumor activity of platinum(II) complexes with histamine and radioiodinated histamine in a transplantable murine adenocarcinoma model
Nuclear medicine and biology, 2008Co-Authors: Piotr Garnuszek, Urszula Karczmarczyk, Michał MaurinAbstract:Abstract Purpose Antitumor activity of the dichloroplatinum(II)–histamine complexes labeled with I-125 or I-131 was investigated in a transplantable murine adenocarcinoma (MA) model. Methods The tumor model was obtained in C3H/W female mice after subcutaneous inoculation of the tumor cells derived from the mice bearing a mammary tumor of spontaneous origin. Antitumor activities of the platinum-histamine complexes were investigated in three independent experiments, which differed in applied doses of preparations (PtCl 2 Hist, PtCl 2 [ 125 I]Hist, PtCl 2 [ 131 I]Hist, PtCl 2 Hist/PtCl 2 [ 125 I]Hist and PtCl 2 Hist/PtCl 2 [ 131 I]Hist), treatment schedules as well as stages of the disease progress in the animals used. Experiment 1 included long-term, multidose treatment with low single doses (treatment duration 31–32 days; 8–10 doses of ca. 0.25∙MTD Pt each). Experiment 2 included short-term, multidose treatment with higher single doses (4×ca. 0.5∙MTD Pt up to Day 13 of the treatment). Experiment 3 included long-term concomitant multidose treatment with higher single doses (9×0.9–0.4∙MTD Pt up to Day 33). Results The long-term treatment with the platinum-histamine preparations revealed inhibiting activity on the tumor growth and size in comparison to control groups. The most intensive and significant antitumor effects were observed for the radioactive complexes. The tumor growth delay factors (GDFs) observed in Experiment 1 were 0.4, 0.7, and 1.2 for PtCl 2 Hist, PtCl 2 Hist/PtCl 2 [ 131 I]Hist, and PtCl 2 Hist/PtCl 2 [ 125 I]Hist, respectively. Significant ( P .05 ) prolongations of median survivals (MS) were found in Experiment 2 following the treatment with higher single doses of PtCl 2 Hist and PtCl 2 His/PtCl 2 [ 125 I]Hist (Ratio MS tr /MS con ca. 1.4). A slightly less potent activity was observed for PtCl 2 Hist/PtCl 2 [ 131 I]Hist, and no survival improvement was found for the groups treated mostly with the radiation (PtCl 2 [ 125 I]Hist and PtCl 2 [ 131 I]Hist). The intensive and long-term concomitant scheduling of the radioactive platinum–histamine complexes labeled with I-125 and I-131 (Experiment 3) resulted in a significant inhibition of the tumor growth (GDF=1.9) and survival prolongation of the tumor-bearing mice (MS tr /MS con =1.5, P =.023). The treatment-related toxicity was mild. Conclusion An enhancement of the antitumor activity due to the multidose concomitant treatment with a combination of cytotoxic/cytostatic dichloroplatinum(II)–histamine and the attached iodine radionuclides was shown in the murine model of Experimental Neoplasm.
Wojciech Kozubski - One of the best experts on this subject based on the ideXlab platform.
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Original article Blood-brain barrier breakdown and cerebellar degeneration in the course of Experimental neoplastic disease. Are circulating Cytokine-Induced Neutrophil Chemoattractant-1 (CINC-1) and -2α(CINC-2α) the involved mediators?
Folia neuropathologica, 2010Co-Authors: Slawomir Michalak, Mieczysław Wender, Grazyna Michałowska-wender, Wojciech KozubskiAbstract:Cerebellar degeneration belongs to indirect effects of malignancy on the nervous system. Although the involvement of immune system is accepted as a hypothesis of its pathology, the clinical observations of ineffective immunomodulatory therapy suggest complex pathomechanisms, which await elucidation. The aim of this study was to prove the blood-brain barrier integrity, its relation to cerebellar degeneration and the role of circulating Cytokine-Induced Neutrophil Chemoattractant-1 (CINC-1) and Cytokine-Induced Neutrophil Chemoattractant-2α (CINC-2α) in indirect effects of Experimental malignancy. Two transplantable Neoplasms: breast cancer (BC) and Morris hepatoma (MH) in rats were used in the study. The blood-brain barrier breakdown was clearly proved in the course of both malignancies. We observed also morphological signs of cerebellar degeneration in both models, with linear loss of Purkinje cells and homogenization changes more pronounced in breast cancer bearing rats. We have found a significant decrease of CINC-1 concentration in serum of rats with growing MH, however BC had no effect on CINC-1 concentration. Changes in serum CINC-2α concentrations in BC did not reach the level of significance, however in MH bearing rats the concentrations increased three weeks after tumour transplantation. In conclusion, we may state that the development of cerebellar degeneration as an indirect effect of Experimental Neoplasm can result from blood-brain barrier (BBB) breakdown and possible passage of neurotoxic factors. The decreased serum concentration of CINC-1 as neuroprotective agent and increased CINC-2α in late stage of MH may be considered for their contribution to cerebellar degeneration.
Urszula Karczmarczyk - One of the best experts on this subject based on the ideXlab platform.
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Antitumor activity of platinum(II) complexes with histamine and radioiodinated histamine in a transplantable murine adenocarcinoma model
Nuclear medicine and biology, 2008Co-Authors: Piotr Garnuszek, Urszula Karczmarczyk, Michał MaurinAbstract:Abstract Purpose Antitumor activity of the dichloroplatinum(II)–histamine complexes labeled with I-125 or I-131 was investigated in a transplantable murine adenocarcinoma (MA) model. Methods The tumor model was obtained in C3H/W female mice after subcutaneous inoculation of the tumor cells derived from the mice bearing a mammary tumor of spontaneous origin. Antitumor activities of the platinum-histamine complexes were investigated in three independent experiments, which differed in applied doses of preparations (PtCl 2 Hist, PtCl 2 [ 125 I]Hist, PtCl 2 [ 131 I]Hist, PtCl 2 Hist/PtCl 2 [ 125 I]Hist and PtCl 2 Hist/PtCl 2 [ 131 I]Hist), treatment schedules as well as stages of the disease progress in the animals used. Experiment 1 included long-term, multidose treatment with low single doses (treatment duration 31–32 days; 8–10 doses of ca. 0.25∙MTD Pt each). Experiment 2 included short-term, multidose treatment with higher single doses (4×ca. 0.5∙MTD Pt up to Day 13 of the treatment). Experiment 3 included long-term concomitant multidose treatment with higher single doses (9×0.9–0.4∙MTD Pt up to Day 33). Results The long-term treatment with the platinum-histamine preparations revealed inhibiting activity on the tumor growth and size in comparison to control groups. The most intensive and significant antitumor effects were observed for the radioactive complexes. The tumor growth delay factors (GDFs) observed in Experiment 1 were 0.4, 0.7, and 1.2 for PtCl 2 Hist, PtCl 2 Hist/PtCl 2 [ 131 I]Hist, and PtCl 2 Hist/PtCl 2 [ 125 I]Hist, respectively. Significant ( P .05 ) prolongations of median survivals (MS) were found in Experiment 2 following the treatment with higher single doses of PtCl 2 Hist and PtCl 2 His/PtCl 2 [ 125 I]Hist (Ratio MS tr /MS con ca. 1.4). A slightly less potent activity was observed for PtCl 2 Hist/PtCl 2 [ 131 I]Hist, and no survival improvement was found for the groups treated mostly with the radiation (PtCl 2 [ 125 I]Hist and PtCl 2 [ 131 I]Hist). The intensive and long-term concomitant scheduling of the radioactive platinum–histamine complexes labeled with I-125 and I-131 (Experiment 3) resulted in a significant inhibition of the tumor growth (GDF=1.9) and survival prolongation of the tumor-bearing mice (MS tr /MS con =1.5, P =.023). The treatment-related toxicity was mild. Conclusion An enhancement of the antitumor activity due to the multidose concomitant treatment with a combination of cytotoxic/cytostatic dichloroplatinum(II)–histamine and the attached iodine radionuclides was shown in the murine model of Experimental Neoplasm.
Slawomir Michalak - One of the best experts on this subject based on the ideXlab platform.
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Original article Blood-brain barrier breakdown and cerebellar degeneration in the course of Experimental neoplastic disease. Are circulating Cytokine-Induced Neutrophil Chemoattractant-1 (CINC-1) and -2α(CINC-2α) the involved mediators?
Folia neuropathologica, 2010Co-Authors: Slawomir Michalak, Mieczysław Wender, Grazyna Michałowska-wender, Wojciech KozubskiAbstract:Cerebellar degeneration belongs to indirect effects of malignancy on the nervous system. Although the involvement of immune system is accepted as a hypothesis of its pathology, the clinical observations of ineffective immunomodulatory therapy suggest complex pathomechanisms, which await elucidation. The aim of this study was to prove the blood-brain barrier integrity, its relation to cerebellar degeneration and the role of circulating Cytokine-Induced Neutrophil Chemoattractant-1 (CINC-1) and Cytokine-Induced Neutrophil Chemoattractant-2α (CINC-2α) in indirect effects of Experimental malignancy. Two transplantable Neoplasms: breast cancer (BC) and Morris hepatoma (MH) in rats were used in the study. The blood-brain barrier breakdown was clearly proved in the course of both malignancies. We observed also morphological signs of cerebellar degeneration in both models, with linear loss of Purkinje cells and homogenization changes more pronounced in breast cancer bearing rats. We have found a significant decrease of CINC-1 concentration in serum of rats with growing MH, however BC had no effect on CINC-1 concentration. Changes in serum CINC-2α concentrations in BC did not reach the level of significance, however in MH bearing rats the concentrations increased three weeks after tumour transplantation. In conclusion, we may state that the development of cerebellar degeneration as an indirect effect of Experimental Neoplasm can result from blood-brain barrier (BBB) breakdown and possible passage of neurotoxic factors. The decreased serum concentration of CINC-1 as neuroprotective agent and increased CINC-2α in late stage of MH may be considered for their contribution to cerebellar degeneration.
