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Xiao-le Wang - One of the best experts on this subject based on the ideXlab platform.
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Prediction of chemotherapeutic response in unresectable non-small-cell lung cancer (NSCLC) patients by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2- (4-sulfophenyl)-2H-tetrazolium (MTS) Assay.
Asian Pacific journal of cancer prevention : APJCP, 2013Co-Authors: Juan Chen, Guo-hua Cheng, Li-pai Chen, Ting-yuan Pang, Xiao-le WangAbstract:Background: Selecting chemotherapy regimens guided by chemosensitivity tests can provide individualized therapies for cancer patients. The 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2Htetrazolium, inner salt (MTS) Assay is one in vitro Assay which has become widely used to evaluate the sensitivity to anticancer agents. The aim of this study was to evaluate the clinical applicability and accuracy of MTS Assay for predicting chemotherapeutic response in unresectable NSCLC patients. Methods: Cancer cells were isolated from malignant pleural effusions of patients by density gradient centrifugation, and their sensitivity to eight chemotherapeutic agents was examined by MTS Assay and compared with clinical response. Results: A total of 37 patients participated in this study, and MTS Assay produced results successfully in 34 patients (91.9%). The sensitivity rates ranged from 8.8% to 88.2%. Twenty-four of 34 patients who received chemotherapy were evaluated for in vitro-in vivo response analysis. The correlation between in vitro chemosensitivity result and in vivo response was highly significant ( P=0.003), and the total predictive accuracy, sensitivity, specificity, positive predictive value, and negative predictive value for MTS Assay were 87.5%, 94.1%, 71.4%, 88.9%, and 83.3%, respectively. The in vitro sensitivity for CDDP also showed a significant correlation with in vivo response (P=0.018, r=0.522). Conclusion: MTS Assay is a preferable in vitro chemosensitivity Assay that could be use to predict the response to chemotherapy and select the appropriate chemotherapy regimens for unresectable NSCLC patients, which could greatly improve therapeutic efficacy and reduce unnecessary adverse effects.
Juan Chen - One of the best experts on this subject based on the ideXlab platform.
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Prediction of chemotherapeutic response in unresectable non-small-cell lung cancer (NSCLC) patients by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2- (4-sulfophenyl)-2H-tetrazolium (MTS) Assay.
Asian Pacific journal of cancer prevention : APJCP, 2013Co-Authors: Juan Chen, Guo-hua Cheng, Li-pai Chen, Ting-yuan Pang, Xiao-le WangAbstract:Background: Selecting chemotherapy regimens guided by chemosensitivity tests can provide individualized therapies for cancer patients. The 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2Htetrazolium, inner salt (MTS) Assay is one in vitro Assay which has become widely used to evaluate the sensitivity to anticancer agents. The aim of this study was to evaluate the clinical applicability and accuracy of MTS Assay for predicting chemotherapeutic response in unresectable NSCLC patients. Methods: Cancer cells were isolated from malignant pleural effusions of patients by density gradient centrifugation, and their sensitivity to eight chemotherapeutic agents was examined by MTS Assay and compared with clinical response. Results: A total of 37 patients participated in this study, and MTS Assay produced results successfully in 34 patients (91.9%). The sensitivity rates ranged from 8.8% to 88.2%. Twenty-four of 34 patients who received chemotherapy were evaluated for in vitro-in vivo response analysis. The correlation between in vitro chemosensitivity result and in vivo response was highly significant ( P=0.003), and the total predictive accuracy, sensitivity, specificity, positive predictive value, and negative predictive value for MTS Assay were 87.5%, 94.1%, 71.4%, 88.9%, and 83.3%, respectively. The in vitro sensitivity for CDDP also showed a significant correlation with in vivo response (P=0.018, r=0.522). Conclusion: MTS Assay is a preferable in vitro chemosensitivity Assay that could be use to predict the response to chemotherapy and select the appropriate chemotherapy regimens for unresectable NSCLC patients, which could greatly improve therapeutic efficacy and reduce unnecessary adverse effects.
Takuo Kuboki - One of the best experts on this subject based on the ideXlab platform.
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Chemical interaction of polyphosphoric acid with titanium and its effect on human bone marrow derived mesenchymal stem cell behavior.
Journal of biomedical materials research. Part A, 2007Co-Authors: Kenji Maekawa, Yasuhiro Yoshida, Atsushi Mine, Takuo Fujisawa, Bart Van Meerbeek, Kazuomi Suzuki, Takuo KubokiAbstract:The aim of this study was to evaluate the effect of treating titanium (Ti) with polyphosphoric acid on the attachment and proliferation of human bone marrow derived mesenchymal stem cells (hBMSCs). Cleaned Ti disks were immersed into three different concentrations of polyphosphoric acid solution (0.1, 1, and 10 wt %) and 10 wt % orthophosphoric acid solution for 24 h at 37°C. Ti immersed in distilled water for 24 h at 37°C served as control. The level of polyphosphoric acid that interacted with the Ti surface was determined by measuring the surface P/Ti ratio (atom%/atom%) using X-ray photoelectron spectroscopy. Degrees of cell attachment (1, 3, 5 h after cell seed) and proliferation (1, 3, 5, and 7 days after cell seed) on each treated Ti disk were evaluated by MTS Assay. The mean surface P/Ti ratios increased in a polyphosphoric acid concentration dependent manner. A significantly higher cell attachment was found on Ti treated with polyphosphoric acid in contrast to untreated Ti (control) for all three culture periods. MTS Assay also revealed that cell proliferation levels significantly increased following a polyphosphoric acid dose dependency. Ti surface treatment with orthophosphoric acid did not influence the cell attachment and proliferation. It was concluded that polyphosphoric acid treatment of Ti enhanced the attachment and proliferation of hBMSCs. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
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Chemical interaction of polyphosphoric acid with titanium and its effect on human bone marrow derived mesenchymal stem cell behavior
Journal of Biomedical Materials Research Part A, 2007Co-Authors: Kenji Maekawa, Yasuhiro Yoshida, Atsushi Mine, Takuo Fujisawa, Kazuomi Suzuki, Bart Van Meerbeek, Takuo KubokiAbstract:The aim of this study was to evaluate the effect of treating titanium (Ti) with polyphosphoric acid on the attachment and proliferation of human bone marrow derived mesenchymal stem cells (hBMSCs). Cleaned Ti disks were immersed into three different concentrations of polyphosphoric acid solution (0.1, 1, and 10 wt %) and 10 wt % orthophosphoric acid solution for 24 h at 37 degrees C. Ti immersed in distilled water for 24 h at 37 degrees C served as control. The level of polyphosphoric acid that interacted with the Ti surface was determined by measuring the surface P/Ti ratio (atom%/atom%) using X-ray photoelectron spectroscopy. Degrees of cell attachment (1, 3, 5 h after cell seed) and proliferation (1, 3, 5, and 7 days after cell seed) on each treated Ti disk were evaluated by MTS Assay. The mean surface P/Ti ratios increased in a polyphosphoric acid concentration dependent manner. A significantly higher cell attachment was found on Ti treated with polyphosphoric acid in contrast to untreated Ti (control) for all three culture periods. MTS Assay also revealed that cell proliferation levels significantly increased following a polyphosphoric acid dose dependency. Ti surface treatment with orthophosphoric acid did not influence the cell attachment and proliferation. It was concluded that polyphosphoric acid treatment of Ti enhanced the attachment and proliferation of hBMSCs.status: publishe
David M. Jablons - One of the best experts on this subject based on the ideXlab platform.
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Wnt inhibitory factor inhibits lung cancer cell growth
The Journal of thoracic and cardiovascular surgery, 2007Co-Authors: Jae Y. Kim, Liang You, Kris Kuchenbecker, Dan J. Raz, David M. JablonsAbstract:Objective Aberrant activation of the Wnt signaling pathway is associated with the pathogenesis of multiple cancers, including non–small cell lung cancer. Wnt inhibitory factor, a secreted Wnt antagonist, is downregulated in non–small cell lung cancer. We hypothesized that restoration of Wnt inhibitory factor function would inhibit lung cancer cell growth. Methods The lung cancer cell lines A549 and H460 were transfected with an expression vector containing the Wnt inhibitory factor gene. Apoptosis rates and colony formation were measured after transfection. Recombinant Wnt inhibitory factor protein was used to treat H460 cells, and proliferation rates were measured with an MTS Assay. Finally, Wnt inhibitory factor plasmid was peritumorally injected near H460 tumor xenografts in nude mice. Results Wnt inhibitory factor–transfected cells had increased apoptosis and decreased colony formation than control cells. Recombinant human Wnt inhibitory factor protein was also able to inhibit H460 cell proliferation measured by using the MTS Assay. Wnt inhibitory factor plasmid significantly inhibited the growth in vivo of H460 tumor xenografts in nude mice. Conclusion These data suggest that Wnt inhibitory factor is able to inhibit lung cancer cell growth both in vitro and in vivo and provides additional evidence that Wnt inhibitory factor plays an important role in Wnt pathway regulation in lung cancer.
Akihiko Gemma - One of the best experts on this subject based on the ideXlab platform.
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Control of the MYC-eIF4E axis plus mTOR inhibitor treatment in small cell lung cancer
BMC cancer, 2015Co-Authors: Masaru Matsumoto, Masahiro Seike, Rintaro Noro, Chie Soeno, Teppei Sugano, Susumu Takeuchi, Akihiko Miyanaga, Kazuhiro Kitamura, Kaoru Kubota, Akihiko GemmaAbstract:Mammalian target of rapamycin (mTOR) inhibitors have anti-tumor effects against renal cell carcinoma, pancreatic neuroendocrine cancer and breast cancer. In this study, we analyzed the antitumor effects of mTOR inhibitors in small cell lung cancer (SCLC) cells and sought to clarify the mechanism of resistance to mTOR inhibitors. We analyzed the antitumor effects of three mTOR inhibitors including everolimus in 7 SCLC cell lines by MTS Assay. Gene-chip analysis, receptor tyrosine kinases (RTK) array and Western blotting analysis were performed to identify molecules associated with resistance to everolimus. Only SBC5 cells showed sensitivity to everolimus by MTS Assay. We established two everolimus resistant-SBC5 cell lines (SBC5 R1 and SBC5 R10) by continuous exposure to increasing concentrations of everolimus stepwise. SPP1 and MYC were overexpressed in both SBC5 R1 and SBC5 R10 by gene-chip analysis. High expression levels of eukaryotic translation initiation factor 4E (eIF4E) were observed in 5 everolimus-resistant SCLC cells and SBC5 R10 cells by Western blotting. MYC siRNA reduced eIF4E phosphorylation in SBC5 cells, suggesting that MYC directly activates eIF4E by an mTOR-independent bypass pathway. Importantly, after reduction of MYC or eIF4E by siRNAs, the SBC5 parent and two SBC5-resistant cells displayed increased sensitivity to everolimus relative to the siRNA controls. These findings suggest that eIF4E has been shown to be an important factor in the resistance to everolimus in SCLC cells. Furthermore, a link between MYC and mTOR-independent eIF4E contribute to the resistance to everolimus in SCLC cells. Control of the MYC-eIF4E axis may be a novel therapeutic strategy for everolimus action in SCLC.