The Experts below are selected from a list of 180 Experts worldwide ranked by ideXlab platform
Gerassimos E. Voutsinas - One of the best experts on this subject based on the ideXlab platform.
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Thymidylate synthase inhibition induces p53-dependent and p53-independent apoptotic responses in human urinary bladder Cancer cells
Journal of Cancer Research and Clinical Oncology, 2011Co-Authors: Dimitrios J. Stravopodis, Panagiotis K. Karkoulis, Eumorphia G. Konstantakou, Sophia Melachroinou, Angeliki Thanasopoulou, Gerasimos Aravantinos, Lukas H. Margaritis, Ema Anastasiadou, Gerassimos E. VoutsinasAbstract:Purpose In search for more effective clinical protocols, the antimetabolite drug 5-fluorouracil (5-FU) has been successfully included in new regimens of bladder Cancer Combination Chemotherapy. In the present study, we have investigated the effects of 5-FU treatment on apoptosis induction in wild-type and mutant p53 urinary bladder Cancer cells. Methods We have used MTT-based assays, FACS analysis, Western blotting and semi-quantitative RT-PCR in RT4 and RT112 (grade I, wild-type p53), as well as in T24 (grade III, mutant p53) and TCCSUP (grade IV, mutant p53) human urinary bladder Cancer cell lines. Results In the urothelial bladder Cancer cell lines RT4 and T24, 5-FU-induced TS inhibition proved to be associated with cell type-dependent (a) sensitivity to the drug, (b) Caspase-mediated apoptosis, (c) p53 stabilization and activation, as well as Rb phosphorylation and E2F1 expression and (d) transcriptional regulation of p53 target genes and their cognate proteins, while an E2F-dependent transcriptional network did not seem to be critically engaged in such type of responses. Conclusions We have shown that in the wild-type p53 context of RT4 cells, 5-FU-triggered apoptosis was prominently efficient and mainly regulated by p53-dependent mechanisms, whereas the mutant p53 environment of T24 cells was able to provide notable levels of resistance to apoptosis, basically ascribed to E2F-independent, and still unidentified, pathways. Nevertheless, the differential vulnerability of RT4 and T24 cells to 5-FU administration could also be associated with cell-type-specific transcriptional expression patterns of certain genes critically involved in 5-FU metabolism.
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Thymidylate synthase inhibition induces p53-dependent and p53-independent apoptotic responses in human urinary bladder Cancer cells.
Journal of cancer research and clinical oncology, 2010Co-Authors: Dimitrios J. Stravopodis, Panagiotis K. Karkoulis, Eumorphia G. Konstantakou, Sophia Melachroinou, Angeliki Thanasopoulou, Gerasimos Aravantinos, Lukas H. Margaritis, Ema Anastasiadou, Gerassimos E. VoutsinasAbstract:In search for more effective clinical protocols, the antimetabolite drug 5-fluorouracil (5-FU) has been successfully included in new regimens of bladder Cancer Combination Chemotherapy. In the present study, we have investigated the effects of 5-FU treatment on apoptosis induction in wild-type and mutant p53 urinary bladder Cancer cells. We have used MTT-based assays, FACS analysis, Western blotting and semi-quantitative RT-PCR in RT4 and RT112 (grade I, wild-type p53), as well as in T24 (grade III, mutant p53) and TCCSUP (grade IV, mutant p53) human urinary bladder Cancer cell lines. In the urothelial bladder Cancer cell lines RT4 and T24, 5-FU-induced TS inhibition proved to be associated with cell type-dependent (a) sensitivity to the drug, (b) Caspase-mediated apoptosis, (c) p53 stabilization and activation, as well as Rb phosphorylation and E2F1 expression and (d) transcriptional regulation of p53 target genes and their cognate proteins, while an E2F-dependent transcriptional network did not seem to be critically engaged in such type of responses. We have shown that in the wild-type p53 context of RT4 cells, 5-FU-triggered apoptosis was prominently efficient and mainly regulated by p53-dependent mechanisms, whereas the mutant p53 environment of T24 cells was able to provide notable levels of resistance to apoptosis, basically ascribed to E2F-independent, and still unidentified, pathways. Nevertheless, the differential vulnerability of RT4 and T24 cells to 5-FU administration could also be associated with cell-type-specific transcriptional expression patterns of certain genes critically involved in 5-FU metabolism.
Dimitrios J. Stravopodis - One of the best experts on this subject based on the ideXlab platform.
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Thymidylate synthase inhibition induces p53-dependent and p53-independent apoptotic responses in human urinary bladder Cancer cells
Journal of Cancer Research and Clinical Oncology, 2011Co-Authors: Dimitrios J. Stravopodis, Panagiotis K. Karkoulis, Eumorphia G. Konstantakou, Sophia Melachroinou, Angeliki Thanasopoulou, Gerasimos Aravantinos, Lukas H. Margaritis, Ema Anastasiadou, Gerassimos E. VoutsinasAbstract:Purpose In search for more effective clinical protocols, the antimetabolite drug 5-fluorouracil (5-FU) has been successfully included in new regimens of bladder Cancer Combination Chemotherapy. In the present study, we have investigated the effects of 5-FU treatment on apoptosis induction in wild-type and mutant p53 urinary bladder Cancer cells. Methods We have used MTT-based assays, FACS analysis, Western blotting and semi-quantitative RT-PCR in RT4 and RT112 (grade I, wild-type p53), as well as in T24 (grade III, mutant p53) and TCCSUP (grade IV, mutant p53) human urinary bladder Cancer cell lines. Results In the urothelial bladder Cancer cell lines RT4 and T24, 5-FU-induced TS inhibition proved to be associated with cell type-dependent (a) sensitivity to the drug, (b) Caspase-mediated apoptosis, (c) p53 stabilization and activation, as well as Rb phosphorylation and E2F1 expression and (d) transcriptional regulation of p53 target genes and their cognate proteins, while an E2F-dependent transcriptional network did not seem to be critically engaged in such type of responses. Conclusions We have shown that in the wild-type p53 context of RT4 cells, 5-FU-triggered apoptosis was prominently efficient and mainly regulated by p53-dependent mechanisms, whereas the mutant p53 environment of T24 cells was able to provide notable levels of resistance to apoptosis, basically ascribed to E2F-independent, and still unidentified, pathways. Nevertheless, the differential vulnerability of RT4 and T24 cells to 5-FU administration could also be associated with cell-type-specific transcriptional expression patterns of certain genes critically involved in 5-FU metabolism.
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Thymidylate synthase inhibition induces p53-dependent and p53-independent apoptotic responses in human urinary bladder Cancer cells.
Journal of cancer research and clinical oncology, 2010Co-Authors: Dimitrios J. Stravopodis, Panagiotis K. Karkoulis, Eumorphia G. Konstantakou, Sophia Melachroinou, Angeliki Thanasopoulou, Gerasimos Aravantinos, Lukas H. Margaritis, Ema Anastasiadou, Gerassimos E. VoutsinasAbstract:In search for more effective clinical protocols, the antimetabolite drug 5-fluorouracil (5-FU) has been successfully included in new regimens of bladder Cancer Combination Chemotherapy. In the present study, we have investigated the effects of 5-FU treatment on apoptosis induction in wild-type and mutant p53 urinary bladder Cancer cells. We have used MTT-based assays, FACS analysis, Western blotting and semi-quantitative RT-PCR in RT4 and RT112 (grade I, wild-type p53), as well as in T24 (grade III, mutant p53) and TCCSUP (grade IV, mutant p53) human urinary bladder Cancer cell lines. In the urothelial bladder Cancer cell lines RT4 and T24, 5-FU-induced TS inhibition proved to be associated with cell type-dependent (a) sensitivity to the drug, (b) Caspase-mediated apoptosis, (c) p53 stabilization and activation, as well as Rb phosphorylation and E2F1 expression and (d) transcriptional regulation of p53 target genes and their cognate proteins, while an E2F-dependent transcriptional network did not seem to be critically engaged in such type of responses. We have shown that in the wild-type p53 context of RT4 cells, 5-FU-triggered apoptosis was prominently efficient and mainly regulated by p53-dependent mechanisms, whereas the mutant p53 environment of T24 cells was able to provide notable levels of resistance to apoptosis, basically ascribed to E2F-independent, and still unidentified, pathways. Nevertheless, the differential vulnerability of RT4 and T24 cells to 5-FU administration could also be associated with cell-type-specific transcriptional expression patterns of certain genes critically involved in 5-FU metabolism.
John R. Murren - One of the best experts on this subject based on the ideXlab platform.
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Progress in the therapy of small cell lung Cancer.
Critical reviews in oncology hematology, 2004Co-Authors: Miklos Simon, Athanassios Argiris, John R. MurrenAbstract:Small cell lung Cancer (SCLC) accounts for approximately 14% of all cases of lung Cancer. Combination Chemotherapy is the most effective treatment modality for SCLC and recently, several new active drugs have emerged. Combinations of platinum agents with CPT-11 or gemcitabine have been successfully compared in phase III trials against the cisplatin/etoposide standard. Modest improvements in the outcome of patients with SCLC have been noted over the last two decades. Thoracic irradiation given concurrently with Chemotherapy improves survival compared with sequential Chemotherapy and radiation, but this approach is associated with more toxicity. Moreover, the optimal doses and fractionation of thoracic irradiation remain to be determined. Three-dimensional treatment planning is under investigation. Prophylactic cranial irradiation (PCI) has established a role in the management of patients who have achieved a complete response to the initial therapy. Novel molecular targeted therapies are among the strategies currently being investigated in SCLC.
Ema Anastasiadou - One of the best experts on this subject based on the ideXlab platform.
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Thymidylate synthase inhibition induces p53-dependent and p53-independent apoptotic responses in human urinary bladder Cancer cells
Journal of Cancer Research and Clinical Oncology, 2011Co-Authors: Dimitrios J. Stravopodis, Panagiotis K. Karkoulis, Eumorphia G. Konstantakou, Sophia Melachroinou, Angeliki Thanasopoulou, Gerasimos Aravantinos, Lukas H. Margaritis, Ema Anastasiadou, Gerassimos E. VoutsinasAbstract:Purpose In search for more effective clinical protocols, the antimetabolite drug 5-fluorouracil (5-FU) has been successfully included in new regimens of bladder Cancer Combination Chemotherapy. In the present study, we have investigated the effects of 5-FU treatment on apoptosis induction in wild-type and mutant p53 urinary bladder Cancer cells. Methods We have used MTT-based assays, FACS analysis, Western blotting and semi-quantitative RT-PCR in RT4 and RT112 (grade I, wild-type p53), as well as in T24 (grade III, mutant p53) and TCCSUP (grade IV, mutant p53) human urinary bladder Cancer cell lines. Results In the urothelial bladder Cancer cell lines RT4 and T24, 5-FU-induced TS inhibition proved to be associated with cell type-dependent (a) sensitivity to the drug, (b) Caspase-mediated apoptosis, (c) p53 stabilization and activation, as well as Rb phosphorylation and E2F1 expression and (d) transcriptional regulation of p53 target genes and their cognate proteins, while an E2F-dependent transcriptional network did not seem to be critically engaged in such type of responses. Conclusions We have shown that in the wild-type p53 context of RT4 cells, 5-FU-triggered apoptosis was prominently efficient and mainly regulated by p53-dependent mechanisms, whereas the mutant p53 environment of T24 cells was able to provide notable levels of resistance to apoptosis, basically ascribed to E2F-independent, and still unidentified, pathways. Nevertheless, the differential vulnerability of RT4 and T24 cells to 5-FU administration could also be associated with cell-type-specific transcriptional expression patterns of certain genes critically involved in 5-FU metabolism.
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Thymidylate synthase inhibition induces p53-dependent and p53-independent apoptotic responses in human urinary bladder Cancer cells.
Journal of cancer research and clinical oncology, 2010Co-Authors: Dimitrios J. Stravopodis, Panagiotis K. Karkoulis, Eumorphia G. Konstantakou, Sophia Melachroinou, Angeliki Thanasopoulou, Gerasimos Aravantinos, Lukas H. Margaritis, Ema Anastasiadou, Gerassimos E. VoutsinasAbstract:In search for more effective clinical protocols, the antimetabolite drug 5-fluorouracil (5-FU) has been successfully included in new regimens of bladder Cancer Combination Chemotherapy. In the present study, we have investigated the effects of 5-FU treatment on apoptosis induction in wild-type and mutant p53 urinary bladder Cancer cells. We have used MTT-based assays, FACS analysis, Western blotting and semi-quantitative RT-PCR in RT4 and RT112 (grade I, wild-type p53), as well as in T24 (grade III, mutant p53) and TCCSUP (grade IV, mutant p53) human urinary bladder Cancer cell lines. In the urothelial bladder Cancer cell lines RT4 and T24, 5-FU-induced TS inhibition proved to be associated with cell type-dependent (a) sensitivity to the drug, (b) Caspase-mediated apoptosis, (c) p53 stabilization and activation, as well as Rb phosphorylation and E2F1 expression and (d) transcriptional regulation of p53 target genes and their cognate proteins, while an E2F-dependent transcriptional network did not seem to be critically engaged in such type of responses. We have shown that in the wild-type p53 context of RT4 cells, 5-FU-triggered apoptosis was prominently efficient and mainly regulated by p53-dependent mechanisms, whereas the mutant p53 environment of T24 cells was able to provide notable levels of resistance to apoptosis, basically ascribed to E2F-independent, and still unidentified, pathways. Nevertheless, the differential vulnerability of RT4 and T24 cells to 5-FU administration could also be associated with cell-type-specific transcriptional expression patterns of certain genes critically involved in 5-FU metabolism.
Panagiotis K. Karkoulis - One of the best experts on this subject based on the ideXlab platform.
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Thymidylate synthase inhibition induces p53-dependent and p53-independent apoptotic responses in human urinary bladder Cancer cells
Journal of Cancer Research and Clinical Oncology, 2011Co-Authors: Dimitrios J. Stravopodis, Panagiotis K. Karkoulis, Eumorphia G. Konstantakou, Sophia Melachroinou, Angeliki Thanasopoulou, Gerasimos Aravantinos, Lukas H. Margaritis, Ema Anastasiadou, Gerassimos E. VoutsinasAbstract:Purpose In search for more effective clinical protocols, the antimetabolite drug 5-fluorouracil (5-FU) has been successfully included in new regimens of bladder Cancer Combination Chemotherapy. In the present study, we have investigated the effects of 5-FU treatment on apoptosis induction in wild-type and mutant p53 urinary bladder Cancer cells. Methods We have used MTT-based assays, FACS analysis, Western blotting and semi-quantitative RT-PCR in RT4 and RT112 (grade I, wild-type p53), as well as in T24 (grade III, mutant p53) and TCCSUP (grade IV, mutant p53) human urinary bladder Cancer cell lines. Results In the urothelial bladder Cancer cell lines RT4 and T24, 5-FU-induced TS inhibition proved to be associated with cell type-dependent (a) sensitivity to the drug, (b) Caspase-mediated apoptosis, (c) p53 stabilization and activation, as well as Rb phosphorylation and E2F1 expression and (d) transcriptional regulation of p53 target genes and their cognate proteins, while an E2F-dependent transcriptional network did not seem to be critically engaged in such type of responses. Conclusions We have shown that in the wild-type p53 context of RT4 cells, 5-FU-triggered apoptosis was prominently efficient and mainly regulated by p53-dependent mechanisms, whereas the mutant p53 environment of T24 cells was able to provide notable levels of resistance to apoptosis, basically ascribed to E2F-independent, and still unidentified, pathways. Nevertheless, the differential vulnerability of RT4 and T24 cells to 5-FU administration could also be associated with cell-type-specific transcriptional expression patterns of certain genes critically involved in 5-FU metabolism.
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Thymidylate synthase inhibition induces p53-dependent and p53-independent apoptotic responses in human urinary bladder Cancer cells.
Journal of cancer research and clinical oncology, 2010Co-Authors: Dimitrios J. Stravopodis, Panagiotis K. Karkoulis, Eumorphia G. Konstantakou, Sophia Melachroinou, Angeliki Thanasopoulou, Gerasimos Aravantinos, Lukas H. Margaritis, Ema Anastasiadou, Gerassimos E. VoutsinasAbstract:In search for more effective clinical protocols, the antimetabolite drug 5-fluorouracil (5-FU) has been successfully included in new regimens of bladder Cancer Combination Chemotherapy. In the present study, we have investigated the effects of 5-FU treatment on apoptosis induction in wild-type and mutant p53 urinary bladder Cancer cells. We have used MTT-based assays, FACS analysis, Western blotting and semi-quantitative RT-PCR in RT4 and RT112 (grade I, wild-type p53), as well as in T24 (grade III, mutant p53) and TCCSUP (grade IV, mutant p53) human urinary bladder Cancer cell lines. In the urothelial bladder Cancer cell lines RT4 and T24, 5-FU-induced TS inhibition proved to be associated with cell type-dependent (a) sensitivity to the drug, (b) Caspase-mediated apoptosis, (c) p53 stabilization and activation, as well as Rb phosphorylation and E2F1 expression and (d) transcriptional regulation of p53 target genes and their cognate proteins, while an E2F-dependent transcriptional network did not seem to be critically engaged in such type of responses. We have shown that in the wild-type p53 context of RT4 cells, 5-FU-triggered apoptosis was prominently efficient and mainly regulated by p53-dependent mechanisms, whereas the mutant p53 environment of T24 cells was able to provide notable levels of resistance to apoptosis, basically ascribed to E2F-independent, and still unidentified, pathways. Nevertheless, the differential vulnerability of RT4 and T24 cells to 5-FU administration could also be associated with cell-type-specific transcriptional expression patterns of certain genes critically involved in 5-FU metabolism.
