The Experts below are selected from a list of 162 Experts worldwide ranked by ideXlab platform
Félix Vargas - One of the best experts on this subject based on the ideXlab platform.
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The pro-oxidant buthionine sulfoximine (BSO) reduces tumor growth of implanted Lewis lung Carcinoma in mice associated with increased protein carbonyl, tubulin abundance, and aminopeptidase activity
Tumor Biology, 2014Co-Authors: Isabel Rodríguez-gómez, Javier Carmona-cortés, Rosemary Wangensteen, Inmaculada Banegas, Ángel M. García-lora, Andrés Quesada, Pablo Vargas-tendero, Félix VargasAbstract:This study evaluated the effects of the pro-oxidant buthionine sulfoximine (BSO) and of the interaction between BSO and TETRAC, an antagonist of αvß3 integrin, on tumor development and aminopeptidase (AP) activity in a murine model of implanted Lewis’s Carcinoma. Male CBA-C57 mice were untreated (controls) or treated with BSO (222 mg/100 mL in drinking water), TETRAC (10 mg/kg/day, i.p.), or BSO + TETRAC. BSO for 28 days and TETRAC were given for the last 20 days. Mice were subcutaneously inoculated with 1 × 10^6 Lewis Carcinoma 3LL cells into the dorsum. Study variables were tumor weight (TW); Hb, as index of tumor-mediated angiogenesis; vascular endothelial growth factor (VEGF) protein abundance; protein carbonyl content; α-tubulin abundance; and GluAp, AlaAp, and AspAp activities. BSO produced a major decrease in TW (203 ± 18 mg) with respect to controls (365 ± 26) and a reduction in Hb content. The TETRAC group also showed marked reductions in TW (129 ± 15) and Hb concentration associated with a reduced VEGF content. The BSO + TETRAC group showed a major TW reduction (125 ± 13); although, the difference with the TETRAC group was not significant. BSO treatment increased protein carbonyl and tubulin abundance in comparison to controls. The activity of all APs was increased in the three experimental groups and was strongly and negatively correlated with TW. In conclusion, administration of BSO reduced the TW, which inversely correlated with protein carbonyl content, suggesting a loss of microtubule polymerization. The finding of a negative correlation between TW and AP activity opens up new perspectives for the study of APs as tumor growth modulators.
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Effect of thyroid hormone–nitric oxide interaction on tumor growth, angiogenesis, and aminopeptidase activity in mice
Tumor Biology, 2014Co-Authors: Javier Carmona-cortés, Isabel Rodríguez-gómez, Rosemary Wangensteen, Inmaculada Banegas, Ángel M. García-lora, Andrés Quesada, Antonio Osuna, Félix VargasAbstract:This study evaluated the effects of thyroid hormone–NO interaction on tumor development, vascularization, vascular endothelial growth factor (VEGF), and aminopeptidase (AP) activity in a murine model of implanted Lewis’s Carcinoma. Experiments were performed in male CBA-C57 mice. Animals were untreated (controls) or treated with: T_4, the antithyroid drug methimazole, the NO inhibitor L-NAME, T_4 + L-NAME, methimazole + NAME, the αvß3 integrin antagonist tetrac, T_4 + tetrac, the iNOS inhibitor aminoguanidine (AG), and T_4 + AG; all treatments were for 6 weeks except for tetrac, administered for the last 11 days. Mice were subcutaneously inoculated with 1 × 10^6 exponentially growing Lewis Carcinoma 3LL cells into the dorsum. Study variables 9 days later were tumor weight (TW), Hb content, an index of tumor vascularization, VEGF, and AP activity. T_4 produced parallel increases in TW and angiogenesis. L-NAME reduced TW and angiogenesis in control, hyperthyroid, and hypothyroid mice, whereas AG had no effect on these variables. Tetrac arrested TW in normal and T_4-treated mice but did not decrease angiogenesis in T_4-treated animals. Negative correlations were found between TW and AP activity in tumors from control hyper- and hypothyroid groups and an inverse relationship was observed between TW and AP activities in tetrac-treated mice. T_4 enhances TW and angiogenesis, in which NO participates, but requires activation of integrin αvß3 to promote carcinogenesis. NO blockade reduces TW, regardless of the thyroid status. Thyroid hormone negatively modulates AP activity in the tumor. Accordingly, blockade of the membrane TH receptor αvß3 integrin reduces TW associated with an increase in AP activity.
Javier Carmona-cortés - One of the best experts on this subject based on the ideXlab platform.
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The pro-oxidant buthionine sulfoximine (BSO) reduces tumor growth of implanted Lewis lung Carcinoma in mice associated with increased protein carbonyl, tubulin abundance, and aminopeptidase activity
Tumor Biology, 2014Co-Authors: Isabel Rodríguez-gómez, Javier Carmona-cortés, Rosemary Wangensteen, Inmaculada Banegas, Ángel M. García-lora, Andrés Quesada, Pablo Vargas-tendero, Félix VargasAbstract:This study evaluated the effects of the pro-oxidant buthionine sulfoximine (BSO) and of the interaction between BSO and TETRAC, an antagonist of αvß3 integrin, on tumor development and aminopeptidase (AP) activity in a murine model of implanted Lewis’s Carcinoma. Male CBA-C57 mice were untreated (controls) or treated with BSO (222 mg/100 mL in drinking water), TETRAC (10 mg/kg/day, i.p.), or BSO + TETRAC. BSO for 28 days and TETRAC were given for the last 20 days. Mice were subcutaneously inoculated with 1 × 10^6 Lewis Carcinoma 3LL cells into the dorsum. Study variables were tumor weight (TW); Hb, as index of tumor-mediated angiogenesis; vascular endothelial growth factor (VEGF) protein abundance; protein carbonyl content; α-tubulin abundance; and GluAp, AlaAp, and AspAp activities. BSO produced a major decrease in TW (203 ± 18 mg) with respect to controls (365 ± 26) and a reduction in Hb content. The TETRAC group also showed marked reductions in TW (129 ± 15) and Hb concentration associated with a reduced VEGF content. The BSO + TETRAC group showed a major TW reduction (125 ± 13); although, the difference with the TETRAC group was not significant. BSO treatment increased protein carbonyl and tubulin abundance in comparison to controls. The activity of all APs was increased in the three experimental groups and was strongly and negatively correlated with TW. In conclusion, administration of BSO reduced the TW, which inversely correlated with protein carbonyl content, suggesting a loss of microtubule polymerization. The finding of a negative correlation between TW and AP activity opens up new perspectives for the study of APs as tumor growth modulators.
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Effect of thyroid hormone–nitric oxide interaction on tumor growth, angiogenesis, and aminopeptidase activity in mice
Tumor Biology, 2014Co-Authors: Javier Carmona-cortés, Isabel Rodríguez-gómez, Rosemary Wangensteen, Inmaculada Banegas, Ángel M. García-lora, Andrés Quesada, Antonio Osuna, Félix VargasAbstract:This study evaluated the effects of thyroid hormone–NO interaction on tumor development, vascularization, vascular endothelial growth factor (VEGF), and aminopeptidase (AP) activity in a murine model of implanted Lewis’s Carcinoma. Experiments were performed in male CBA-C57 mice. Animals were untreated (controls) or treated with: T_4, the antithyroid drug methimazole, the NO inhibitor L-NAME, T_4 + L-NAME, methimazole + NAME, the αvß3 integrin antagonist tetrac, T_4 + tetrac, the iNOS inhibitor aminoguanidine (AG), and T_4 + AG; all treatments were for 6 weeks except for tetrac, administered for the last 11 days. Mice were subcutaneously inoculated with 1 × 10^6 exponentially growing Lewis Carcinoma 3LL cells into the dorsum. Study variables 9 days later were tumor weight (TW), Hb content, an index of tumor vascularization, VEGF, and AP activity. T_4 produced parallel increases in TW and angiogenesis. L-NAME reduced TW and angiogenesis in control, hyperthyroid, and hypothyroid mice, whereas AG had no effect on these variables. Tetrac arrested TW in normal and T_4-treated mice but did not decrease angiogenesis in T_4-treated animals. Negative correlations were found between TW and AP activity in tumors from control hyper- and hypothyroid groups and an inverse relationship was observed between TW and AP activities in tetrac-treated mice. T_4 enhances TW and angiogenesis, in which NO participates, but requires activation of integrin αvß3 to promote carcinogenesis. NO blockade reduces TW, regardless of the thyroid status. Thyroid hormone negatively modulates AP activity in the tumor. Accordingly, blockade of the membrane TH receptor αvß3 integrin reduces TW associated with an increase in AP activity.
Isabel Rodríguez-gómez - One of the best experts on this subject based on the ideXlab platform.
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The pro-oxidant buthionine sulfoximine (BSO) reduces tumor growth of implanted Lewis lung Carcinoma in mice associated with increased protein carbonyl, tubulin abundance, and aminopeptidase activity
Tumor Biology, 2014Co-Authors: Isabel Rodríguez-gómez, Javier Carmona-cortés, Rosemary Wangensteen, Inmaculada Banegas, Ángel M. García-lora, Andrés Quesada, Pablo Vargas-tendero, Félix VargasAbstract:This study evaluated the effects of the pro-oxidant buthionine sulfoximine (BSO) and of the interaction between BSO and TETRAC, an antagonist of αvß3 integrin, on tumor development and aminopeptidase (AP) activity in a murine model of implanted Lewis’s Carcinoma. Male CBA-C57 mice were untreated (controls) or treated with BSO (222 mg/100 mL in drinking water), TETRAC (10 mg/kg/day, i.p.), or BSO + TETRAC. BSO for 28 days and TETRAC were given for the last 20 days. Mice were subcutaneously inoculated with 1 × 10^6 Lewis Carcinoma 3LL cells into the dorsum. Study variables were tumor weight (TW); Hb, as index of tumor-mediated angiogenesis; vascular endothelial growth factor (VEGF) protein abundance; protein carbonyl content; α-tubulin abundance; and GluAp, AlaAp, and AspAp activities. BSO produced a major decrease in TW (203 ± 18 mg) with respect to controls (365 ± 26) and a reduction in Hb content. The TETRAC group also showed marked reductions in TW (129 ± 15) and Hb concentration associated with a reduced VEGF content. The BSO + TETRAC group showed a major TW reduction (125 ± 13); although, the difference with the TETRAC group was not significant. BSO treatment increased protein carbonyl and tubulin abundance in comparison to controls. The activity of all APs was increased in the three experimental groups and was strongly and negatively correlated with TW. In conclusion, administration of BSO reduced the TW, which inversely correlated with protein carbonyl content, suggesting a loss of microtubule polymerization. The finding of a negative correlation between TW and AP activity opens up new perspectives for the study of APs as tumor growth modulators.
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Effect of thyroid hormone–nitric oxide interaction on tumor growth, angiogenesis, and aminopeptidase activity in mice
Tumor Biology, 2014Co-Authors: Javier Carmona-cortés, Isabel Rodríguez-gómez, Rosemary Wangensteen, Inmaculada Banegas, Ángel M. García-lora, Andrés Quesada, Antonio Osuna, Félix VargasAbstract:This study evaluated the effects of thyroid hormone–NO interaction on tumor development, vascularization, vascular endothelial growth factor (VEGF), and aminopeptidase (AP) activity in a murine model of implanted Lewis’s Carcinoma. Experiments were performed in male CBA-C57 mice. Animals were untreated (controls) or treated with: T_4, the antithyroid drug methimazole, the NO inhibitor L-NAME, T_4 + L-NAME, methimazole + NAME, the αvß3 integrin antagonist tetrac, T_4 + tetrac, the iNOS inhibitor aminoguanidine (AG), and T_4 + AG; all treatments were for 6 weeks except for tetrac, administered for the last 11 days. Mice were subcutaneously inoculated with 1 × 10^6 exponentially growing Lewis Carcinoma 3LL cells into the dorsum. Study variables 9 days later were tumor weight (TW), Hb content, an index of tumor vascularization, VEGF, and AP activity. T_4 produced parallel increases in TW and angiogenesis. L-NAME reduced TW and angiogenesis in control, hyperthyroid, and hypothyroid mice, whereas AG had no effect on these variables. Tetrac arrested TW in normal and T_4-treated mice but did not decrease angiogenesis in T_4-treated animals. Negative correlations were found between TW and AP activity in tumors from control hyper- and hypothyroid groups and an inverse relationship was observed between TW and AP activities in tetrac-treated mice. T_4 enhances TW and angiogenesis, in which NO participates, but requires activation of integrin αvß3 to promote carcinogenesis. NO blockade reduces TW, regardless of the thyroid status. Thyroid hormone negatively modulates AP activity in the tumor. Accordingly, blockade of the membrane TH receptor αvß3 integrin reduces TW associated with an increase in AP activity.
Lisete Ribeiro Teixeira - One of the best experts on this subject based on the ideXlab platform.
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A modified experimental model of malignant pleural disease induced by lung Lewis Carcinoma (LLC) cells
Journal of Translational Medicine, 2015Co-Authors: Milena Marques Pagliarelli Acencio, Juliana Puka, Evaldo Marchi, Leila Antonangelo, Ricardo Mingarini Terra, Francisco Suso Vargas, Vera Luiza Capelozzi, Lisete Ribeiro TeixeiraAbstract:Background Malignant pleural effusion resulting mainly from pleural metastases of lung adenoCarcinoma has clinical relevance, being a sign of poor prognosis and low life expectancy. Experimental models can mimic the human condition, contributing to advances in current understanding of the mechanisms patients’ pleural fluid accumulation and possible therapeutic strategies. The objective of this study is to evaluate the role of different concentrations of Lewis lung Carcinoma cells (LLC cells) at the time of induction of experimental MPE and the main effects on survival of animals. Methods C57BL/6 mice received intrapleural injection of 0.1, 0.5 or 1.5 × 10^5 LLC cells and survival curve, biochemical and pathological analyses of pleural fluid and tissue were analyzed. Results Evaluation of weight loss, mobility and survival showed that animals that received 0.5 × 10^5 cells maintained more stable condition up to day 14 and a gain of 6 days survival over mice that received the highest concentration. Conclusion This study may allow a better understanding the mechanisms involved in the development of malignant pleural effusion and it may be promising in evaluating therapy to avoid recurrence, as the best time to indicate pleurodesis or target therapies.
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A modified experimental model of malignant pleural disease induced by lung Lewis Carcinoma (LLC) cells
Journal of translational medicine, 2015Co-Authors: Milena Marques Pagliarelli Acencio, Juliana Puka, Evaldo Marchi, Leila Antonangelo, Ricardo Mingarini Terra, Francisco Suso Vargas, Vera Luiza Capelozzi, Lisete Ribeiro TeixeiraAbstract:Background Malignant pleural effusion resulting mainly from pleural metastases of lung adenoCarcinoma has clinical relevance, being a sign of poor prognosis and low life expectancy. Experimental models can mimic the human condition, contributing to advances in current understanding of the mechanisms patients’ pleural fluid accumulation and possible therapeutic strategies. The objective of this study is to evaluate the role of different concentrations of Lewis lung Carcinoma cells (LLC cells) at the time of induction of experimental MPE and the main effects on survival of animals.
M. M. Fomina - One of the best experts on this subject based on the ideXlab platform.
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The Antitumor Activity of Dinitrosyl Iron Complexes with Mercaptosuccinate in Murine Solid Tumor Models
Biophysics, 2019Co-Authors: A. F. Vanin, D. B. Korman, L. A. Ostrovskaya, N. V. Bluchterova, V. A. Rykova, M. M. FominaAbstract:The antitumor activity of the binuclear form of dinitrosyl iron complexes with mercaptosuccinate administered intravenously was studied in murine models of solid tumors: Lewis lung Carcinoma and Acatol adenoCarcinoma. The maximum effect, suppression of tumor growth by 65% in comparison to the control for Lewis Carcinoma, was observed for a course of six intravenous injections in a daily dose of 2.5 μM/kg administered every 2 or 3 days over the period of days 1–17 after tumor transplantation.
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The antitumor effect of dinitrosyl iron complexes with glutathione in a murine solid-tumor model
Biophysics, 2017Co-Authors: A. F. Vanin, D. B. Korman, L. A. Ostrovskaya, V. A. Rykova, N. V. Blyuchterova, M. M. FominaAbstract:A significant antitumor activity of aqueous solutions of binuclear dinitrosyl iron complexes with glutathione was found when they were injected intravenously in a model of a solid malignant tumor, that is, Lewis Carcinoma, in mice. Dinitrosyl iron complexes completely inhibited the tumor growth (by 100%) at doses of 20, 10, and 2 μmol/kg in the first 11 days after the beginning of experiment followed by tumor proliferation at a rate that was lowest for the lowest of the used doses. At day 16, the inhibition of tumor growth was 90% when a solution of dinitrosyl iron complexes was injected at a dose of 2 μmol/kg five times with an interval of 2 to 3 days between injections; whereas the inhibition of tumor growth did not exceed 70 and 30% at doses of 10 and 20 μmol/kg, respectively. Acceleration, rather than inhibition of Carcinoma growth was observed at a dose of 100 μmol/kg. The tumor weight increased 1.5–2.0 times compared to the control values, depending on the time.