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Wojciech P Mielicki - One of the best experts on this subject based on the ideXlab platform.
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arsenic trioxide downregulates Cancer Procoagulant activity in mcf 7 and wm 115 cell lines in vitro
Wspolczesna Onkologia-Contemporary Oncology, 2015Co-Authors: Ewelina Hoffman, Katarzyna Gizelska, Marek Mirowski, Wojciech P MielickiAbstract:THE AIM OF THE STUDY: To analyze human breast Cancer cell line MCF-7 and human malignant melanoma cell line WM-115 in order to characterize the cellular expression of CP and to evaluate whether ATO may affect this activity, as well as the viability of the cells. MATERIAL AND METHODS: The inhibitory effect of arsenic trioxide on the proliferation of MCF-7 and WM-115 cells were measured with MTT test. The activity of Cancer Procoagulant after ATO exposure was determined by a specific three-stage chromogenic assay. RESULTS: ATO decreased the CP activity in a dose- and time-dependent manner in MCF-7 cells with no effect on cell proliferation at the same time. However, it affected the CP activity of WM-115 cells in a different way. Reduction in CP activity was followed by an increase after 48 h incubation. The cells viability results showed dose-and time-correlated response within high arsenic concentrations. CONCLUSIONS: Arsenic trioxide downregulates the CP expression in human breast Cancer and melanoma cells.
Mielicki Wojciech - One of the best experts on this subject based on the ideXlab platform.
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Arsenic trioxide downregulates Cancer Procoagulant activity in MCF-7 and WM-115 cell lines in vitro
'Termedia Sp. z.o.o.', 2015Co-Authors: Hoffman, Ewelina A, Gizelska Katarzyna, Mirowski Marek, Mielicki WojciechAbstract:© 2015 Termedia Sp. z o. o. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (http://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.THE AIM OF THE STUDY: To analyze human breast Cancer cell line MCF-7 and human malignant melanoma cell line WM-115 in order to characterize the cellular expression of CP and to evaluate whether ATO may affect this activity, as well as the viability of the cells.MATERIAL AND METHODS: The inhibitory effect of arsenic trioxide on the proliferation of MCF-7 and WM-115 cells were measured with MTT test. The activity of Cancer Procoagulant after ATO exposure was determined by a specific three-stage chromogenic assay.RESULTS: ATO decreased the CP activity in a dose- and time-dependent manner in MCF-7 cells with no effect on cell proliferation at the same time. However, it affected the CP activity of WM-115 cells in a different way. Reduction in CP activity was followed by an increase after 48 h incubation. The cells viability results showed dose-and time-correlated response within high arsenic concentrations.CONCLUSIONS: Arsenic trioxide downregulates the CP expression in human breast Cancer and melanoma cells.Peer reviewedFinal Published versio
Rousseau Aurélie - One of the best experts on this subject based on the ideXlab platform.
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Contribution de la modélisation des propriétés coagulantes de cellules cancéreuses dans la compréhension de leurs mécanismes d 'action et dans l 'étude de l'éfficacité des agents anticoagulants
HAL CCSD, 2016Co-Authors: Rousseau AurélieAbstract:Aims: study of influence of pancreas adenocarcinoma cells (BXPC3) and human breast carcinoma cells (MCF7) on the antithrombotic efficiency of apixaban, fondaparinux and enoxaparin. Dissection of Procoagulant mechanisms of BXPC3 and MCF7.Methods: Cells were cultured and adhered in 96-well plates. Normal platelet poor or rich plasma were spiked whit apixaban, fondaparinux or enoxaparin. Thrombin generation (TG) was done with CAT¨ assay in different conditions. Alternatively spliced TF (asTF), TF activity (TFa) and Cancer Procoagulant (CP) were assessed. Primary human umbilical vein cells (HUVEC) were used as normal control.Results: Comparison on the basis of IC50 showed that in the presence of BXPC3 or MCF7 the efficiency of apixaban was preserved. Fondaparinux was more vulnerable to the presence of Cancer cells. The TFa and asTF were found in abundant amounts in BXCP3 than MCF7 cells. TG enhancement by BXPC3 and MCF7 was mediated by FVII. Factor XII was more important for TG enhancement by MCF7.The presence of MPs drastically increases the generation of thrombin and this effect depending of the type of their original cells.Conclusion: The type of Cancer cells is determinant for the antithrombotic efficiency of the specific factor Xa inhibitors. The mechanism of activation of blood coagulation by the BXPC3 is dominated by the TF pathway, MCF7 additionally imply also FXII activation. The hypercoagulability induced by Cancer cells is the resultant of the combination of the Procoagulant properties of Cancer cells with Procoagulant elements of the plasma microenvironment and highlight that circulating MVs are key players in the pathogenesis of Cancer-associated thrombosis.Objectifs: Etude de l'influence des cellules du pancréas d'adénocarcinome (BXPC3) et des cellules de carcinome du sein humain (MCF7) sur l'efficacité antithrombotique de l'apixaban, du fondaparinux et de l'énoxaparine. Recherche des mécanismes Procoagulants des BXPC3 et MCF7.Méthodes: Les cellules sont cultivées sur plaques 96 puits. Un plasma normal pauvre ou riche en plaquettes est surchargé par des anticoagulants. La génération de thrombine (GT) est réalisée dans différentes conditions par le test CAT. Le facteur tissulaire alternatif épissé (asTF), l'activité du FT (FTa) et le Cancer Procoagulant (CP) sont évalués. Les cellules HUVEC servent de contrôle normal.Résultats: La comparaison sur la base de l’IC50 a montré qu'en présence de BXPC3 ou de MCF7, l'efficacité de l'apixaban a été préservée. Le fondaparinux est plus vulnérable par la présence de cellules cancéreuses. Le FTa et l’asTF sont plus abondants pour les BXPC3 que les cellules MCF7. La GT est médiée plus fortement par le FVII pour les BXPC3 que les MCF7. Le facteur XII était plus important pour la GT médiée par les MCF7. La présence de MPs augmente considérablement la production de thrombine et cet effet est fonction du type de cellules et leur origine.Conclusion: Le type de cellules cancéreuses est déterminant pour l'efficacité anti-thrombotique des inhibiteurs spécifiques du facteur Xa. La GT par les BXPC3 est dominée par la voie du FT. Le rôle du FXII est plus impliqué pour les MCF7. L'hypercoagulabilité induite par les cellules cancéreuses est la résultante de la combinaison des propriétés Procoagulantes des cellules cancéreuses elles-mêmes et des éléments Procoagulants du microenvironnement
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Contribution of the modeling of the coagulant properties of Cancer cells in the understanding of their mechanisms of action and in the study of the efficiency of anticoagulant agents
2016Co-Authors: Rousseau AurélieAbstract:Objectifs: Etude de l'influence des cellules du pancréas d'adénocarcinome (BXPC3) et des cellules de carcinome du sein humain (MCF7) sur l'efficacité antithrombotique de l'apixaban, du fondaparinux et de l'énoxaparine. Recherche des mécanismes Procoagulants des BXPC3 et MCF7.Méthodes: Les cellules sont cultivées sur plaques 96 puits. Un plasma normal pauvre ou riche en plaquettes est surchargé par des anticoagulants. La génération de thrombine (GT) est réalisée dans différentes conditions par le test CAT. Le facteur tissulaire alternatif épissé (asTF), l'activité du FT (FTa) et le Cancer Procoagulant (CP) sont évalués. Les cellules HUVEC servent de contrôle normal.Résultats: La comparaison sur la base de l’IC50 a montré qu'en présence de BXPC3 ou de MCF7, l'efficacité de l'apixaban a été préservée. Le fondaparinux est plus vulnérable par la présence de cellules cancéreuses. Le FTa et l’asTF sont plus abondants pour les BXPC3 que les cellules MCF7. La GT est médiée plus fortement par le FVII pour les BXPC3 que les MCF7. Le facteur XII était plus important pour la GT médiée par les MCF7. La présence de MPs augmente considérablement la production de thrombine et cet effet est fonction du type de cellules et leur origine.Conclusion: Le type de cellules cancéreuses est déterminant pour l'efficacité anti-thrombotique des inhibiteurs spécifiques du facteur Xa. La GT par les BXPC3 est dominée par la voie du FT. Le rôle du FXII est plus impliqué pour les MCF7. L'hypercoagulabilité induite par les cellules cancéreuses est la résultante de la combinaison des propriétés Procoagulantes des cellules cancéreuses elles-mêmes et des éléments Procoagulants du microenvironnement.Aims: study of influence of pancreas adenocarcinoma cells (BXPC3) and human breast carcinoma cells (MCF7) on the antithrombotic efficiency of apixaban, fondaparinux and enoxaparin. Dissection of Procoagulant mechanisms of BXPC3 and MCF7.Methods: Cells were cultured and adhered in 96-well plates. Normal platelet poor or rich plasma were spiked whit apixaban, fondaparinux or enoxaparin. Thrombin generation (TG) was done with CAT¨ assay in different conditions. Alternatively spliced TF (asTF), TF activity (TFa) and Cancer Procoagulant (CP) were assessed. Primary human umbilical vein cells (HUVEC) were used as normal control.Results: Comparison on the basis of IC50 showed that in the presence of BXPC3 or MCF7 the efficiency of apixaban was preserved. Fondaparinux was more vulnerable to the presence of Cancer cells. The TFa and asTF were found in abundant amounts in BXCP3 than MCF7 cells. TG enhancement by BXPC3 and MCF7 was mediated by FVII. Factor XII was more important for TG enhancement by MCF7.The presence of MPs drastically increases the generation of thrombin and this effect depending of the type of their original cells.Conclusion: The type of Cancer cells is determinant for the antithrombotic efficiency of the specific factor Xa inhibitors. The mechanism of activation of blood coagulation by the BXPC3 is dominated by the TF pathway, MCF7 additionally imply also FXII activation. The hypercoagulability induced by Cancer cells is the resultant of the combination of the Procoagulant properties of Cancer cells with Procoagulant elements of the plasma microenvironment and highlight that circulating MVs are key players in the pathogenesis of Cancer-associated thrombosis
Ewelina Hoffman - One of the best experts on this subject based on the ideXlab platform.
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arsenic trioxide downregulates Cancer Procoagulant activity in mcf 7 and wm 115 cell lines in vitro
Wspolczesna Onkologia-Contemporary Oncology, 2015Co-Authors: Ewelina Hoffman, Katarzyna Gizelska, Marek Mirowski, Wojciech P MielickiAbstract:THE AIM OF THE STUDY: To analyze human breast Cancer cell line MCF-7 and human malignant melanoma cell line WM-115 in order to characterize the cellular expression of CP and to evaluate whether ATO may affect this activity, as well as the viability of the cells. MATERIAL AND METHODS: The inhibitory effect of arsenic trioxide on the proliferation of MCF-7 and WM-115 cells were measured with MTT test. The activity of Cancer Procoagulant after ATO exposure was determined by a specific three-stage chromogenic assay. RESULTS: ATO decreased the CP activity in a dose- and time-dependent manner in MCF-7 cells with no effect on cell proliferation at the same time. However, it affected the CP activity of WM-115 cells in a different way. Reduction in CP activity was followed by an increase after 48 h incubation. The cells viability results showed dose-and time-correlated response within high arsenic concentrations. CONCLUSIONS: Arsenic trioxide downregulates the CP expression in human breast Cancer and melanoma cells.
Hoffman, Ewelina A - One of the best experts on this subject based on the ideXlab platform.
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Arsenic trioxide downregulates Cancer Procoagulant activity in MCF-7 and WM-115 cell lines in vitro
'Termedia Sp. z.o.o.', 2015Co-Authors: Hoffman, Ewelina A, Gizelska Katarzyna, Mirowski Marek, Mielicki WojciechAbstract:© 2015 Termedia Sp. z o. o. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (http://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.THE AIM OF THE STUDY: To analyze human breast Cancer cell line MCF-7 and human malignant melanoma cell line WM-115 in order to characterize the cellular expression of CP and to evaluate whether ATO may affect this activity, as well as the viability of the cells.MATERIAL AND METHODS: The inhibitory effect of arsenic trioxide on the proliferation of MCF-7 and WM-115 cells were measured with MTT test. The activity of Cancer Procoagulant after ATO exposure was determined by a specific three-stage chromogenic assay.RESULTS: ATO decreased the CP activity in a dose- and time-dependent manner in MCF-7 cells with no effect on cell proliferation at the same time. However, it affected the CP activity of WM-115 cells in a different way. Reduction in CP activity was followed by an increase after 48 h incubation. The cells viability results showed dose-and time-correlated response within high arsenic concentrations.CONCLUSIONS: Arsenic trioxide downregulates the CP expression in human breast Cancer and melanoma cells.Peer reviewedFinal Published versio
