Search results for: sorafenib

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id="custom-search-input"> <div class="input-group"> <i class="fas fa-search"></i> <input type="text" class="search-query" name="q" placeholder="Author, Title, Abstract, Keywords" value="sorafenib"> <input type="submit" class="btn_search" value="Search"> </div> </div> </form> </div> </div> <div class="row mt-3"> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Commenced</strong> in January 2007</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Frequency:</strong> Monthly</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Edition:</strong> International</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Paper Count:</strong> 5</div> </div> </div> </div> <h1 class="mt-3 mb-3 text-center" style="font-size:1.6rem;">Search results for: sorafenib</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">5</span> The Effects of Metformin And PCL-sorafenib Nanoparticles Co-treatment on MCF-7 Cell Culture Model of Breast Cancer</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Emad%20Heydarnia">Emad Heydarnia</a>, <a href="https://publications.waset.org/abstracts/search?q=Aref%20Sepasi"> Aref Sepasi</a>, <a href="https://publications.waset.org/abstracts/search?q=Nika%20Asefi"> Nika Asefi</a>, <a href="https://publications.waset.org/abstracts/search?q=Sara%20Khakshournia"> Sara Khakshournia</a>, <a href="https://publications.waset.org/abstracts/search?q=Javad%20Mohammadnejad"> Javad Mohammadnejad</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Despite breakthrough therapeutics in breast cancer, it is one of the main causes of mortality among women worldwide. Thus, drug therapies for treating breast cancer have recently been developed by scientists. Metformin and Sorafenib are well-known therapeutic in breast cancer. In the present study, we combined Sorafenib and PCL-sorafenib with metformin to improve drug absorption and promote therapeutic efficiency. Methods: The MCF-7 cells were treated with Metformin, Sorafenib, or PCL-sorafenib. The growth inhibitory effect of these drugs and cell viability were assessed using MTT and flow cytometry assays, respectively. The expression of targeted genes involved in cell proliferation, signaling, and the cell cycle was measured by Real-time PCR. Results: The results showed that MCF-7 cells treated with Metformin/Sorafenib and PCL-sorafenib/Metformin co-treatment contributed to 50% viability compared to untreated group. Moreover, PI and Annexin V staining tests showed that the cells viability for Metformin/Sorafenib and PCL-sorafenib/Metformin was 38% and 17%, respectively. Furthermore, Sorafenib/Metformin and PCL-sorafenib/Metformin leads to p53 gene expression increase by which they can increase ROS, thereby decreasing GPX4 gene expression. In addition, they affected the expression of BCL2, and BAX genes and altered the cell cycle. Conclusion: Together, the combination of PCL-sorafenib/Metformin and Sorafenib/Metformin increased Sorafenib absorption at lower doses and also leads to apoptosis and oxidative stress increases in MCF-7 cells. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=breast%20cancer" title="breast cancer">breast cancer</a>, <a href="https://publications.waset.org/abstracts/search?q=metformin" title=" metformin"> metformin</a>, <a href="https://publications.waset.org/abstracts/search?q=nanotechnology" title=" nanotechnology"> nanotechnology</a>, <a href="https://publications.waset.org/abstracts/search?q=sorafenib" title=" sorafenib"> sorafenib</a> </p> <a href="https://publications.waset.org/abstracts/183789/the-effects-of-metformin-and-pcl-sorafenib-nanoparticles-co-treatment-on-mcf-7-cell-culture-model-of-breast-cancer" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/183789.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">72</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4</span> The Effect of Sorafenibe on Soat1 Protein by Using Molecular Docking Method</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Mahdiyeh%20Gholaminezhad">Mahdiyeh Gholaminezhad</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Context: The study focuses on the potential impact of Sorafenib on SOAT1 protein in liver cancer treatment, addressing the need for more effective therapeutic options. Research aim: To explore the effects of Sorafenib on the activity of SOAT1 protein in liver cancer cells. Methodology: Molecular docking was employed to analyze the interaction between Sorafenib and SOAT1 protein. Findings: The study revealed a significant effect of Sorafenib on the stability and activity of SOAT1 protein, suggesting its potential as a treatment for liver cancer. Theoretical importance: This research highlights the molecular mechanism underlying Sorafenib's anti-cancer properties, contributing to the understanding of its therapeutic effects. Data collection: Data on the molecular structure of Sorafenib and SOAT1 protein were obtained from computational simulations and databases. Analysis procedures: Molecular docking simulations were performed to predict the binding interactions between Sorafenib and SOAT1 protein. Question addressed: How does Sorafenib influence the activity of SOAT1 protein and what are the implications for liver cancer treatment? Conclusion: The study demonstrates the potential of Sorafenib as a targeted therapy for liver cancer by affecting the activity of SOAT1 protein. Reviewers' Comments: The study provides valuable insights into the molecular basis of Sorafenib's action on SOAT1 protein, suggesting its therapeutic potential. To enhance the methodology, the authors could consider validating the docking results with experimental data for further validation. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=liver%20cancer" title="liver cancer">liver cancer</a>, <a href="https://publications.waset.org/abstracts/search?q=sorafenib" title=" sorafenib"> sorafenib</a>, <a href="https://publications.waset.org/abstracts/search?q=SOAT1" title=" SOAT1"> SOAT1</a>, <a href="https://publications.waset.org/abstracts/search?q=molecular%20docking" title=" molecular docking"> molecular docking</a> </p> <a href="https://publications.waset.org/abstracts/189263/the-effect-of-sorafenibe-on-soat1-protein-by-using-molecular-docking-method" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/189263.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">26</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3</span> The Effect of Thymoquinone and Sorafenib Combination on Hepatocellular Carcinoma Cell Line</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Nabila%20N.%20El-Maraghy">Nabila N. El-Maraghy</a>, <a href="https://publications.waset.org/abstracts/search?q=Amany%20Essa"> Amany Essa</a>, <a href="https://publications.waset.org/abstracts/search?q=Yousra%20Abdel%E2%80%93Mottaleb"> Yousra Abdel鈥揗ottaleb</a>, <a href="https://publications.waset.org/abstracts/search?q=Nada%20Ismail"> Nada Ismail</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The use of combination of chemotherapy and natural products to influence the cell death with low doses of chemotherapeutic agents and few side effects has recently emerged as a new method of cancer therapy. Aim: Evaluation the modulatory effect of Thymoquinone on HepG2 cells treated with Sorafenib. Methods: Hepatocellular Carcinoma HepG2 cell line was treated with Sorafenib and TQ individually and in combination. The effect of these treatments on cell viability (MTT assay), apoptosis (Expression of Caspase-3) and oxidative markers (GSH content and extent of lipid peroxidation) was determined. Results: When compared the effect of both agents alone and the combination of the IC50 of Sorafenib and the IC50 TQ, the combination resulted in reduction of cell inhibition and apoptosis and antagonize their actions on GSH content and extent of lipid peroxidation which are increased. This study showed potent anti-tumor activity of both TQ and Sorafenib separately on HepG2 but upon combination surprisingly they interacted and give antagonistic effect. Conclusion: Co-treatment resulted in antagonistic interaction between Sorafenib and Thymoquinone. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=antagonism" title="antagonism">antagonism</a>, <a href="https://publications.waset.org/abstracts/search?q=hepatocellular%20carcinoma" title=" hepatocellular carcinoma"> hepatocellular carcinoma</a>, <a href="https://publications.waset.org/abstracts/search?q=sorafenib" title=" sorafenib"> sorafenib</a>, <a href="https://publications.waset.org/abstracts/search?q=thymoquinone" title=" thymoquinone "> thymoquinone </a> </p> <a href="https://publications.waset.org/abstracts/48191/the-effect-of-thymoquinone-and-sorafenib-combination-on-hepatocellular-carcinoma-cell-line" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/48191.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">554</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">2</span> Computational Investigation of V599 Mutations of BRAF Protein and Its Control over the Therapeutic Outcome under the Malignant Condition</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Mayank">Mayank</a>, <a href="https://publications.waset.org/abstracts/search?q=Navneet%20Kaur"> Navneet Kaur</a>, <a href="https://publications.waset.org/abstracts/search?q=Narinder%20Singh"> Narinder Singh</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The V599 mutations in the BRAF protein are extremely oncogenic, responsible for countless of malignant conditions. Along with wild type, V599E, V599D, and V599R are the important mutated variants of the BRAF proteins. The BRAF inhibitory anticancer agents are continuously developing, and sorafenib is a BRAF inhibitor that is under clinical use. The crystal structure of sorafenib bounded to wild type, and V599 is known, showing a similar interaction pattern in both the case. The mutated 599th residue, in both the case, is also found not interacting directly with the co-crystallized sorafenib molecule. However, the IC50 value of sorafenib was found extremely different in both the case, i.e., 22 nmol/L for wild and 38 nmol/L for V599E protein. Molecular docking study and MMGBSA binding energy results also revealed a significant difference in the binding pattern of sorafenib in both the case. Therefore, to explore the role of distinctively situated 599th residue, we have further conducted comprehensive computational studies. The molecular dynamics simulation, residue interaction network (RIN) analysis, and residue correlation study results revealed the importance of the 599th residue on the therapeutic outcome and overall dynamic of the BRAF protein. Therefore, although the position of 599th residue is very much distinctive from the ligand-binding cavity of BRAF, still it has exceptional control over the overall functional outcome of the protein. The insight obtained here may seem extremely important and guide us while designing ideal BRAF inhibitory anticancer molecules. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=BRAF" title="BRAF">BRAF</a>, <a href="https://publications.waset.org/abstracts/search?q=oncogenic" title=" oncogenic"> oncogenic</a>, <a href="https://publications.waset.org/abstracts/search?q=sorafenib" title=" sorafenib"> sorafenib</a>, <a href="https://publications.waset.org/abstracts/search?q=computational%20studies" title=" computational studies"> computational studies</a> </p> <a href="https://publications.waset.org/abstracts/117283/computational-investigation-of-v599-mutations-of-braf-protein-and-its-control-over-the-therapeutic-outcome-under-the-malignant-condition" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/117283.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">115</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">1</span> Substituted Thiazole Analogues as Anti-Tumor Agents</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Menna%20Ewida">Menna Ewida</a>, <a href="https://publications.waset.org/abstracts/search?q=Dalal%20Abou%20El-Ella"> Dalal Abou El-Ella</a>, <a href="https://publications.waset.org/abstracts/search?q=Dina%20Lasheen"> Dina Lasheen</a>, <a href="https://publications.waset.org/abstracts/search?q=Huessin%20El-Subbagh"> Huessin El-Subbagh</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: Vascular Endothelial Growth Factor receptor (VEGF) is a signal protein produced by cells that stimulates vasculogenesis to create new blood vessels. VEGF family binds to three trans-membrane tyrosine kinase receptors,Dihydrofolate reductase (DHFR) is an enzyme of crucial importance in medicinal chemistry. DHFR catalyzes the reduction 7,8 dihydro-folate to tetrahydrofolate and intimately couples with thymidylate synthase which is a pivotal enzyme that catalysis the reductive methylation of deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP) utilizing N5,N10-methylene tetrahydrofolate as a cofactor which functions as the source of the methyl group. Purpose: Novel substituted Thiazole agents were designed as DHFR and VEGF-TK inhibitors with increased synergistic activity and decreased side effects. Methods: Five series of compounds were designed with a rational that mimic the pharmacophoric features present in the reported active compounds that target DHFR & VEGFR. These molecules were docked against Methotrexate & Sorafenib as controls. An in silico ADMET study was also performed to validate the bioavailability of the newly designed compounds. The in silico molecular docking & ADMET study were also applied to the non-classical antifolates for comparison. The interaction energy comparable to that of MTX for DHFRI and Sorafenib for VEGF-TKI activity were recorded. Results: Compound 5 exhibited the highest interaction energy when docked against Sorafenib, While Compound 9 showed the highest interaction energy when docked against MTX with the perfect binding mode. Comparable results were also obtained for the ADMET study. Most of the compounds showed absorption within (95-99) zone which varies according to the type of substituents. Conclusions: The Substituted Thiazole Analogues could be a suitable template for antitumor drugs that possess enhanced bioavailability and act as DHFR and VEGF-TK inhibitors. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=anti-tumor%20agents" title="anti-tumor agents">anti-tumor agents</a>, <a href="https://publications.waset.org/abstracts/search?q=DHFR" title=" DHFR"> DHFR</a>, <a href="https://publications.waset.org/abstracts/search?q=drug%20design" title=" drug design"> drug design</a>, <a href="https://publications.waset.org/abstracts/search?q=molecular%20modeling" title=" molecular modeling"> molecular modeling</a>, <a href="https://publications.waset.org/abstracts/search?q=VEGFR-TKIs" title=" VEGFR-TKIs"> VEGFR-TKIs</a> </p> <a href="https://publications.waset.org/abstracts/52650/substituted-thiazole-analogues-as-anti-tumor-agents" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/52650.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">235</span> </span> </div> </div> </div> </main> <footer> <div id="infolinks" class="pt-3 pb-2"> <div class="container"> <div style="background-color:#f5f5f5;" class="p-3"> <div class="row"> <div class="col-md-2"> <ul class="list-unstyled"> About <li><a href="https://waset.org/page/support">About Us</a></li> <li><a href="https://waset.org/page/support#legal-information">Legal</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/WASET-16th-foundational-anniversary.pdf">WASET celebrates its 16th foundational anniversary</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Account <li><a href="https://waset.org/profile">My Account</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Explore <li><a href="https://waset.org/disciplines">Disciplines</a></li> <li><a href="https://waset.org/conferences">Conferences</a></li> <li><a href="https://waset.org/conference-programs">Conference Program</a></li> <li><a href="https://waset.org/committees">Committees</a></li> <li><a href="https://publications.waset.org">Publications</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Research <li><a href="https://publications.waset.org/abstracts">Abstracts</a></li> <li><a href="https://publications.waset.org">Periodicals</a></li> <li><a href="https://publications.waset.org/archive">Archive</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Open Science <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Science-Philosophy.pdf">Open Science Philosophy</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Science-Award.pdf">Open Science Award</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Society-Open-Science-and-Open-Innovation.pdf">Open Innovation</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Postdoctoral-Fellowship-Award.pdf">Postdoctoral Fellowship Award</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Scholarly-Research-Review.pdf">Scholarly Research Review</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Support <li><a href="https://waset.org/page/support">Support</a></li> <li><a href="https://waset.org/profile/messages/create">Contact Us</a></li> <li><a href="https://waset.org/profile/messages/create">Report Abuse</a></li> </ul> </div> </div> </div> </div> </div> <div class="container text-center"> <hr style="margin-top:0;margin-bottom:.3rem;"> <a href="https://creativecommons.org/licenses/by/4.0/" target="_blank" class="text-muted small">Creative Commons Attribution 4.0 International License</a> <div id="copy" class="mt-2">© 2024 World Academy of Science, Engineering and Technology</div> </div> </footer> <a href="javascript:" id="return-to-top"><i class="fas fa-arrow-up"></i></a> <div class="modal" id="modal-template"> <div class="modal-dialog"> <div class="modal-content"> <div class="row m-0 mt-1"> <div class="col-md-12"> <button type="button" class="close" data-dismiss="modal" aria-label="Close"><span aria-hidden="true">×</span></button> </div> </div> <div class="modal-body"></div> </div> </div> </div> <script src="https://cdn.waset.org/static/plugins/jquery-3.3.1.min.js"></script> <script src="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/js/bootstrap.bundle.min.js"></script> <script src="https://cdn.waset.org/static/js/site.js?v=150220211556"></script> <script> jQuery(document).ready(function() { /*jQuery.get("https://publications.waset.org/xhr/user-menu", function (response) { jQuery('#mainNavMenu').append(response); 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Search results for: sorafenib