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Sunitinib - Crossref

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Last Updated: 18 July 2022

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Novel electrospun implants of Sunitinib can depress ex-vivo ocular neovascularization

One of the key signs of Wet Age-related Macular Degeneration and DiabeticRetinopathy, which involves the neovascularization of choroidal neovascularization is the occurrence of neoangiogenic i. e. The retinal layer is protruding from the choroidal blood vessels and protruding through the retinal layer.

Source link: https://doi.org/10.5920/bjpharm.1174


Phase 2 clinical trial of sunitinib as adjunctive treatment in patients with advanced differentiated thyroid cancer

Objective The aim of this study was to assess the efficacy and safety of sunitinib following at least one course of radioactive iodine therapy in patients with advanced differentiated thyroid cancer patients. The study's endpoints included the highest response rate and progression-free survival in Solid Tumors 1. 1, analysis of serum thyroglobulin, and toxic assessment. In total, 23 patients were enrolled and were treated with a 37. 5 mg sunitinib oral dose that began daily and was used in daily doses. Conclusions The mean best response was a decrease of 17. 2% in tumor sum from baseline, down by 17. 2%. Six patients had partial response, and 13 had stable disease with a 72 percent prevalence of clinical benefit, with an average mortality of 83%. There was no statistically significant difference between the baseline and post-treatment Tg values between the medians of the baseline and post-treatment Tg levels. Conclusions These results show that sunitinib has a significant anti-tumor activity in patients with advanced DTC.

Source link: https://doi.org/10.1530/eje-15-0930


Sunitinib achieved fast and sustained control of VIPoma symptoms

Two patients with progressive metastatic pancreatic NETs and refractory VIPoma signs were treated with sunitinib. In both cases, sunitinib discontinuation led to a rapid outbreak of watery diarrhea, which resolved in a few days after reintroducing sunitinib. The anti-tumor effects of sunitinib on VIPoma syndrome was undoubtedly not related to any anti-tumor mechanism. Multiple-tyrosine kinase receptor blockadenib-driven inhibition of multiple sunitinib can act on clandestine pathways and reveal sunitinib's ability to enhance VIPoma symptoms. Sunitinib may be a medical alternative to treat refractory VIPoma symptoms in patients with NETs.

Source link: https://doi.org/10.1530/eje-14-0682


Cost–effectiveness analysis of nivolumab plus cabozantinib versus sunitinib as first-line therapy in advanced renal cell carcinoma

From a U. S. payer perspective, Aim: To determine the cost-effectiveness of first-line treatment for advanced renal cell carcinoma with nivolumab plus cabozantinib versus sunitinib. Conclusion: From a U. S. payer's viewpoint, first-line nivolumab plus cabozantinib for advanced renal cell carcinoma is not cost-effective, so it is not cost-effective.

Source link: https://doi.org/10.2217/imt-2021-0156


Dramatic radiographic response resulting in cerebrospinal fluid rhinorrhea associated with sunitinib therapy in recurrent atypical meningioma: case report

A recent clinical trial of sunitinib for treatment of recurrent Grade II and III meningiomas showed promising outcomes in this population, but only 2 patients had significant radiographic responses, with tumor volume reduction. Within weeks of initiating therapy, the Institution of sunitinib therapy produced a dramatic radiographic response, with marked reduction in the tumor volume and reduction of brainstem vasogenic edema. The important radiographic evidence of tumor formation in the clival zone was also associated with CSF rhinorrhea as a result of the completion of the aggressive skull base meningioma, which necessitated stopping the sunitinib cream. Sunitinib has been shown promising therapeutic success in carefully selected patients with recurrent atypical meningiomas where conventional approaches have been ineffective. CSF rhinorrhea is a risk associated with CSF rhinorrrhea, particularly in more invasive skull base lesions that have a dramatic radiographic response.

Source link: https://doi.org/10.3171/2016.9.jns161629


CircME1 promotes aerobic glycolysis and sunitinib resistance of clear cell renal cell carcinoma through cis-regulation of ME1

Abstract Circular RNAs play a vital role in cell renal cell carcinoma apopulation. We found circME1, a novel circRNA that aids in sunitinib resistance development in ccRCC, herein. In addition, a ME1 specific inhibitor could be able to inhibit the circME1's oncogenic functions. Our findings, which can be used for anticancer therapy, reveal that the circME1/ME1 pathway plays a role in both ccRCC growth and sunitinib resistance formation.

Source link: https://doi.org/10.1038/s41388-022-02386-8


Sunitinib Reduced the Migration of Ectopic Endometrial Cells via p-VEGFR-PI3K-AKT-YBX1-Snail Signaling Pathway

Sunitinib plays a significant role in migration, as shown by our latest reports. Patients were divided into two groups: the control group and the sunitinib group. The result was as expected, with p-VEGFR, PI3K, AKT, YBX1, and snail being measured in the control group and sunitinib group and the VEGFR+sunitinib group. By immunofluorescence, we found sunitinib reduced the number of heterotopic foci and reduced the number of heterotopic foci, YBX1, and snail. sunitinib's migration of ectopic endometrial cells with the presence of the p-VEGFR-PI3K-Snail signaling pathway in both in vitro and in vivo experiments was reduced in both in vitro and in vivo experiments. Sunitinib, according to this report, is a potential target drug for EMs therapy.

Source link: https://doi.org/10.1155/2022/6042518


Abstract 983: A dual inhibitor of MDR-1 and ABCG2,elacridar, enhances cytotoxic effects of sunitinib on RCC cell lines.

Abstract Sunitinib is a multi-targeted receptor tyrosine kinase inhibitor that is currently approved for use in advanced renal cell carcinoma. We found that by elacridar, we suggested that inhibition of MDR transporters by elacridar could overcome sunitinib resistance in experimental RCC. The cells were treated with sunitinib alone, elacridar alone, or the mixture, and MTT's cytotoxicity analysis was determined by the MTT cytotoxicity test. MDR-1 and ABCG2 mRNA and protein were identified by real time RT-PCR or Western blotting, according to MDR-1 and ABCG2 mRNA and their protein. Assay's P-gp functional test, MCF-7 cells were used as a negative control for the P-gp functional assay. Our findings showed that elacridar significantly enhanced sunitinib cytotoxicity in RCC cells. These results show that sunitinib resistance is partially mediated by MDR transporter gene and protein expression. Sunitinib's cytotoxic effects on RCC cell lines can be enhanced by a dual inhibitor of MDR-1 and ABCG2, elacridar.

Source link: https://doi.org/10.1158/1538-7445.am2013-983


Abstract 965: Establishment of a Sunitinib resistant cell line from ccRCC by long term drug application.

Abstract: Sunitinib is a multitargeted tyrosine kinase inhibitor involved in the treatment of advanced renal cell carcinoma. We began to investigate SUN's effectiveness in long-term cell culture studies using permanent cell lines representing ccRCC. To help elucidate the mechanism behind SUN's failure, we began to investigate the mechanism behind SUN's death. As a result of f proliferation-inhibition, cell lines in ccRCC cell lines show a decrease in viability down to 40% at 2-5 percent at 2-5'u03bcM/L SUN-dependent on cell type and cell concentration. Long-term application of SUN to these ccRCC-cells cells led to no inhibition of proliferation at 2-5 bcM/l, according to SUN-insensitive cell clones that have no inhibition of proliferation at this ccRCC-cells drug. Conclusion: Drug resistance following a long-term SUN treatment provides cell lines to study the molecular mechanisms responsible for this phenomenon. Establishment of a Sunitinib resistant cell line from ccRCC by long-term drug use. In:: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research, 2013-04-10; Washington, DC; September 6-10.

Source link: https://doi.org/10.1158/1538-7445.am2013-965


Abstract 5641: Sunitinib inhibits AXL phosphorylation in tumor cells.

Abstract Background Sunitinib is a multi-targeted tyrosine kinase inhibitor that is used for the treatment of patients with advanced renal cell cancer. Drug resistance to sunitinib is a common medical problem. We therefore investigated Axl's potential involvement in sunitinib resistance. Methods 786-O cells resistant to sunitinib were obtained by continued exposure to the drug as previously reported. By RT-PCR and Western blot, AXL expression was investigated in 786-O cell lines and EC-RF24 endothelial cells. MTT cell viability assays determined the sensitivity of cells transfected with siRNAs against AXL and AXL inhibitor R428 to MXL or scrambled siRNAs. Conclusions Axl phosphorylation in vitro in both 786-O and EC-RF24 cells was dose-dependently inhibited by sunitinib, with a 50% inhibitory concentration of 5 u03bcM. Activity of recombinant Axl kinase was determined on tyrosine-containing peptide arrays in the presence of 0,1 or 4 u03bcM R428. In addition, 786-O sunitinib resistant cells had a 4-fold increase in Axl protein relative to 786-O parental cells. However, gene silencing of AXL in 786-O SUN cells by RNA interference did not sensitize the cells to sunitinib, but it did not sensitize them to sunitinib. With respective IC50 values of 0. 9 u03bcM and 1. 8 bcM, Sunitinib-resistant cells were shown to be cross-resistant to the Axl inhibitor R428 with respective IC50 values of 0. 9 bcM and 1. 8 bcM. Despite overexpression of sunitinib-resistant cells, AXL's gene silencing of 786-O resistant cells did not enable them to sunitinib, demonstrating that sunitinib resistance is not mediated by AXL. In tumor cells, Sunitinib blocks AXL phosphorylation.

Source link: https://doi.org/10.1158/1538-7445.am2013-5641

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions