PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33650658-0 2021 Circadian clock protein CRY1 prevents paclitaxel-induced senescence of bladder cancer cells by promoting p53 degradation. Paclitaxel 38-48 tumor protein p53 Homo sapiens 105-108 33650658-11 2021 These data suggested that the accumulated CRY1 in cisplatin-resistant cells could prevent PTX-induced senescence by promoting p53 degradation. Paclitaxel 90-93 tumor protein p53 Homo sapiens 126-129 32237067-0 2020 PBK attenuates paclitaxel-induced autophagic cell death by suppressing p53 in H460 non-small cell lung cancer cells. Paclitaxel 15-25 tumor protein p53 Homo sapiens 71-74 33363381-0 2020 UBE2N Regulates Paclitaxel Sensitivity of Ovarian Cancer via Fos/P53 Axis. Paclitaxel 16-26 tumor protein p53 Homo sapiens 65-68 33072537-0 2020 Restoring of miR-193a-5p Sensitizes Breast Cancer Cells to Paclitaxel through P53 Pathway. Paclitaxel 59-69 tumor protein p53 Homo sapiens 78-81 33072537-4 2020 Therefore, the aim of this study was to evaluate the potential function of miR-193a-5p and paclitaxel in the apoptosis induction by targeting P53 in BC cells. Paclitaxel 91-101 tumor protein p53 Homo sapiens 142-145 32632453-4 2020 Here, we established two paclitaxel (PTX)-resistant TNBC cancer cell lines using an intermittent and stepwise method and found that long non-coding RNA long intergenic non-protein-coding RNA p53-induced transcript (LINC-PINT) was significantly decreased in PTX-resistant cancer cells. Paclitaxel 25-35 tumor protein p53 Homo sapiens 191-194 32632453-4 2020 Here, we established two paclitaxel (PTX)-resistant TNBC cancer cell lines using an intermittent and stepwise method and found that long non-coding RNA long intergenic non-protein-coding RNA p53-induced transcript (LINC-PINT) was significantly decreased in PTX-resistant cancer cells. Paclitaxel 37-40 tumor protein p53 Homo sapiens 191-194 32722340-0 2020 TP53 Mutation Analysis in Gastric Cancer and Clinical Outcomes of Patients with Metastatic Disease Treated with Ramucirumab/Paclitaxel or Standard Chemotherapy. Paclitaxel 124-134 tumor protein p53 Homo sapiens 0-4 32722340-6 2020 In the Ramucirumab/Paclitaxel group, 29/48 (60.4%) patients had TP53 mutations. Paclitaxel 19-29 tumor protein p53 Homo sapiens 64-68 33002289-0 2021 Gallic acid potentiates the apoptotic effect of paclitaxel and carboplatin via overexpression of Bax and P53 on the MCF-7 human breast cancer cell line. Paclitaxel 48-58 tumor protein p53 Homo sapiens 105-108 33363381-15 2020 Furthermore, reversed regulation of Fos and P53 based on UBE2N reduction could reverse paclitaxel sensitivity, respectively. Paclitaxel 87-97 tumor protein p53 Homo sapiens 44-47 33363381-16 2020 Conclusion: Our study suggests that UBE2N could be used as a therapeutic agent for paclitaxel-resistant ovarian cancer through Fos/P53 pathway. Paclitaxel 83-93 tumor protein p53 Homo sapiens 131-134 32238452-0 2020 Duloxetine attenuates paclitaxel-induced peripheral nerve injury by inhibiting p53-related pathways. Paclitaxel 22-32 tumor protein p53 Homo sapiens 79-82 32237067-5 2020 Moreover, p53 expression facilitated an increase in the LC3-II/ LC3-I ratio in response to paclitaxel, and PBK knockdown augmented paclitaxel-mediated p53 transcriptional activity. Paclitaxel 91-101 tumor protein p53 Homo sapiens 10-13 32237067-5 2020 Moreover, p53 expression facilitated an increase in the LC3-II/ LC3-I ratio in response to paclitaxel, and PBK knockdown augmented paclitaxel-mediated p53 transcriptional activity. Paclitaxel 131-141 tumor protein p53 Homo sapiens 151-154 32237067-6 2020 Meanwhile, paclitaxel induced PBK-mediated p53 nuclear export and its subsequent ubiquitination in control cells, but not in PBK knockdown cells. Paclitaxel 11-21 tumor protein p53 Homo sapiens 43-46 32237067-7 2020 We conclude that PBK hampers paclitaxel-induced autophagic cell death by suppressing p53, suggesting a potential role of PBK in p53-mediated H460 cell death. Paclitaxel 29-39 tumor protein p53 Homo sapiens 85-88 32237067-7 2020 We conclude that PBK hampers paclitaxel-induced autophagic cell death by suppressing p53, suggesting a potential role of PBK in p53-mediated H460 cell death. Paclitaxel 29-39 tumor protein p53 Homo sapiens 128-131 31391192-0 2019 6-Phosphofructo-2-Kinase/Fructose-2,6-Biphosphatase-2 Regulates TP53-Dependent Paclitaxel Sensitivity in Ovarian and Breast Cancers. Paclitaxel 79-89 tumor protein p53 Homo sapiens 64-68 32401925-4 2020 Results demonstrated that beta-elemene+paclitaxel induced apoptosis of SKOV3 cells, down-regulated anti-apoptotic Bcl-2 and Bcl-xl gene expression and up-regulated pro-apoptotic P53 and Apaf1 gene expression in SKOV3 cells. Paclitaxel 39-49 tumor protein p53 Homo sapiens 178-181 31648639-7 2020 Furthermore, Ag@PTX enhanced the anti-canceractivity of A549 cells through ROS-mediated p53 and AKT signalling pathways. Paclitaxel 16-19 tumor protein p53 Homo sapiens 88-91 31819616-0 2019 Low-Concentration PTX And RSL3 Inhibits Tumor Cell Growth Synergistically By Inducing Ferroptosis In Mutant p53 Hypopharyngeal Squamous Carcinoma. Paclitaxel 18-21 tumor protein p53 Homo sapiens 108-111 31819616-3 2019 Recent findings showed low-concentration paclitaxel (PTX) could inhibit cell death by upregulating p53 expression; downregulating glutaminolysis-related genes. Paclitaxel 41-51 tumor protein p53 Homo sapiens 99-102 31819616-3 2019 Recent findings showed low-concentration paclitaxel (PTX) could inhibit cell death by upregulating p53 expression; downregulating glutaminolysis-related genes. Paclitaxel 53-56 tumor protein p53 Homo sapiens 99-102 31783991-2 2019 METHODS: To describe topological features of the MTAs networks associated to intrinsic apoptosis induction in p53-null prostate cancer cells, we predicted and compared the interactomes and topological properties of Paclitaxel and Vincristine, and thus, the essential nodes corresponding with the pro- and anti-apoptotic proteins and their kinetics were subjected to experimental analysis in PC-3 cell line. Paclitaxel 215-225 tumor protein p53 Homo sapiens 110-113 31783991-3 2019 RESULTS: The essential nodes of the apoptotic pathways, TP53, and CASP3, were identified in both, Paclitaxel and Vincristine networks, but the intrinsic pathway markers BCL2, BAX, and BCL2L1 were identified as hub nodes only in the Paclitaxel network. Paclitaxel 98-108 tumor protein p53 Homo sapiens 56-60 31783991-3 2019 RESULTS: The essential nodes of the apoptotic pathways, TP53, and CASP3, were identified in both, Paclitaxel and Vincristine networks, but the intrinsic pathway markers BCL2, BAX, and BCL2L1 were identified as hub nodes only in the Paclitaxel network. Paclitaxel 232-242 tumor protein p53 Homo sapiens 56-60 31068300-10 2019 RRM1 silencing significantly inhibited the proliferation (P &lt; 0.01) and enhanced the apoptosis-inducing effect of paclitaxel in MCF-7/R cells (P &lt; 0.001); RRM1 silencing also resulted in obviously reduced Akt phosphorylation, suppressed Bcl-2 expression and promoted the expression of p53 protein in MCF-7/R cells. Paclitaxel 121-131 tumor protein p53 Homo sapiens 299-302 31088908-0 2019 HIF Inactivation of p53 in Ovarian Cancer Can Be Reversed by Topotecan, Restoring Cisplatin and Paclitaxel Sensitivity. Paclitaxel 96-106 tumor protein p53 Homo sapiens 20-23 31379992-10 2019 Also, the analysis correlated with induced cell death elucidated that concurrent treatment of polysaccharide plus paclitaxel had a further anti-cancer effect against A2780cp cells mainly through restoration of p53 and mitochondrial apoptosis cell death induction. Paclitaxel 114-124 tumor protein p53 Homo sapiens 210-213 31452796-9 2019 In summary, shikonin can sensitize esophageal cancer cells to paclitaxel-treatment by promoting cell mitotic arrest and reinforcing the susceptibility of esophageal cancer cells to apoptosis induced by paclitaxel, which is potentially associated with altered levels of Bcl-2 and p53. Paclitaxel 62-72 tumor protein p53 Homo sapiens 279-282 31171918-6 2019 Results: Our results revealed that the highest cytotoxic effect, the highest induction of apoptosis and significant elevation in P53 and Caspase 3 levels was seen in Paclitaxel/Gallic acid combination. Paclitaxel 166-176 tumor protein p53 Homo sapiens 129-132 30592172-14 2019 CONCLUSION: Paclitaxel can significantly repress cell proliferation and induce apoptosis of HS 737.T cells through activating Caspase-3, PARP1, p53, and TP53INP1. Paclitaxel 12-22 tumor protein p53 Homo sapiens 144-147 30628717-8 2019 Further experiments validated that p53 enhanced the sensitivity of NCI-H1299 cells to Taxol through initiating the caspase-3 and -9 intrinsic death pathways, and resulted in cell cycle arrest at the G1/S phases. Paclitaxel 86-91 tumor protein p53 Homo sapiens 35-38 29980405-5 2018 Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisplatin, irinotecan, oxaliplatin, and paclitaxel increased significantly. Paclitaxel 232-242 tumor protein p53 Homo sapiens 28-32 28884602-13 2018 Expression analysis by real-time PCR showed the significant up-regulation of two tumour suppressor genes, P53 and P21 in response to combination of silibinin and paclitaxel. Paclitaxel 162-172 tumor protein p53 Homo sapiens 106-109 30173893-0 2018 Paclitaxel promotes lung cancer cell apoptosis via MEG3-P53 pathway activation. Paclitaxel 0-10 tumor protein p53 Homo sapiens 56-59 30173893-10 2018 PTX significantly inhibited the proliferation of NSCLC cells and increased the expressions of MEG3 and P53. Paclitaxel 0-3 tumor protein p53 Homo sapiens 103-106 30173893-13 2018 Our results suggest that the MEG3-P53 pathway is involved in the apoptosis of A549 cells induced by PTX. Paclitaxel 100-103 tumor protein p53 Homo sapiens 34-37 30592172-9 2019 RNA-seq and bioinformatics analysis showed that apoptosis, death receptor signaling pathway, TNF signaling pathway, and TP53 regulated transcription of cell death genes pathway were closely associated with paclitaxel in the treatment of GCTB. Paclitaxel 206-216 tumor protein p53 Homo sapiens 120-124 30592172-10 2019 Western bolt results revealed that paclitaxel induced cleavage of Caspase-3 and PARP1, and increased the phosphorylation level of p53 in HS 737.T cells. Paclitaxel 35-45 tumor protein p53 Homo sapiens 130-133 27994465-7 2016 Furthermore, Ag@PEI@PTX enhanced cytotoxic effects on HepG2 cells and triggered intracellular reactive oxygen species; the signaling pathways of AKT, p53, and MAPK were activated to advance cell apoptosis. Paclitaxel 20-23 tumor protein p53 Homo sapiens 150-153 29684847-5 2018 RESULTS: Cell lines and tumor cells p53+, p53- revealed a significant decrease in cell survival after camptothecin, paclitaxel, cisplatin treatment, compared to the control group (p < 0.01). Paclitaxel 116-126 tumor protein p53 Homo sapiens 36-39 29334216-2 2018 The particle size and the zeta potential of PTX-DODAB/p53-rHDL nanoparticles were 177.2 nm and -20.06 mV, respectively. Paclitaxel 44-47 tumor protein p53 Homo sapiens 54-57 29203914-2 2018 Our objective was to engender synthetic lethality to paclitaxel (PTX), the frontline treatment for endometrial cancer, in tumours with mutant p53 and enhance the therapeutic efficacy using polymeric nanoparticles (NPs). Paclitaxel 53-63 tumor protein p53 Homo sapiens 142-145 29203914-2 2018 Our objective was to engender synthetic lethality to paclitaxel (PTX), the frontline treatment for endometrial cancer, in tumours with mutant p53 and enhance the therapeutic efficacy using polymeric nanoparticles (NPs). Paclitaxel 65-68 tumor protein p53 Homo sapiens 142-145 29203914-6 2018 Together, our data provide compelling evidence for future studies of BIBF- and PTX-loaded NPs as a therapeutic opportunity for LOF p53 cancers. Paclitaxel 79-82 tumor protein p53 Homo sapiens 131-134 28869866-3 2017 In order to overcome these limitations, an oncolytic Ad expressing a p53 variant (oAd-vp53) that is resistant to p53 inactivation in the tumor microenvironment was complexed with PEGylated and PTX-conjugated polymeric micelle (APP). Paclitaxel 193-196 tumor protein p53 Homo sapiens 69-72 28522974-11 2017 Up-regulation of p53 and p21 in colorectal carcinoma cells treated with low-dose PTX also contributed to inhibition of tumor cell growth. Paclitaxel 81-84 tumor protein p53 Homo sapiens 17-20 29727353-11 2018 Only paclitaxel-treated ovarian cancer cells showed decrease in expression of p53. Paclitaxel 5-15 tumor protein p53 Homo sapiens 78-81 29684847-5 2018 RESULTS: Cell lines and tumor cells p53+, p53- revealed a significant decrease in cell survival after camptothecin, paclitaxel, cisplatin treatment, compared to the control group (p < 0.01). Paclitaxel 116-126 tumor protein p53 Homo sapiens 42-45 29684847-6 2018 In p53+ group, the expression of Ser20 significantly increased after camptothecin and paclitaxel (p < 0.05). Paclitaxel 86-96 tumor protein p53 Homo sapiens 3-6 29373839-5 2018 NgBR knockdown enhanced paclitaxel-induced cell apoptosis by modulating expression of p53 and survivin in ERalpha positive breast cancer cells via NgBR-mediated PI3K/Akt and MAPK/ERK signaling pathways. Paclitaxel 24-34 tumor protein p53 Homo sapiens 86-89 27764550-0 2016 Paclitaxel-induced aberrant mitosis and mitotic slippage efficiently lead to proliferative death irrespective of canonical apoptosis and p53. Paclitaxel 0-10 tumor protein p53 Homo sapiens 137-140 27191893-6 2016 However, when stratified by chemotherapy regimen, patients whose tumors had TP53 and HR mutations demonstrated a marked survival advantage when treated with platinum and paclitaxel vs. platinum +/- cyclophosphamide (median OS of 90 months (95% CI 50-NA) vs. 29.5 months (95% CI 17.7-50.5), p = 0.0005). Paclitaxel 170-180 tumor protein p53 Homo sapiens 76-80 27779649-5 2016 Results indicated that curcumin combined with paclitaxel decreased c-Ha-Ras, Rho-A, p53 and Bcl-xL gene expression in comparison to control and substances alone in MCF-7 cell line. Paclitaxel 46-56 tumor protein p53 Homo sapiens 84-87 27779649-11 2016 Curcumin alone and combined with paclitaxel increased p53, Bid, caspase-3, caspase-8 and Bax gene expression in MDA-MB-231, whereas Bcl-xL decreased such expression in MDA-MB-231 cells. Paclitaxel 33-43 tumor protein p53 Homo sapiens 54-57 27431785-8 2016 This study demonstrates that the combination of NCS and PTX can potentiate the effect on survival and apoptosis of glioma cells via suppression of Akt, bcl-2, and activations of p53; Meanwhile, the in vivo studies also confirmed that the combination of NCS and PTX synergistically inhibit the gliom growth. Paclitaxel 56-59 tumor protein p53 Homo sapiens 178-181 27304668-0 2016 Glaucarubinone sensitizes KB cells to paclitaxel by inhibiting ABC transporters via ROS-dependent and p53-mediated activation of apoptotic signaling pathways. Paclitaxel 38-48 tumor protein p53 Homo sapiens 102-105 27304668-9 2016 Importantly, GLU and/or PTX triggered apoptosis through the activation of pro-apoptotic proteins such as p53, Bax, and caspase-9. Paclitaxel 24-27 tumor protein p53 Homo sapiens 105-108 26309162-7 2015 Moreover, h-R3-dendriplexes for p53 delivery indicated efficient cell growth inhibition and potentiated paclitaxel-induced cell death. Paclitaxel 104-114 tumor protein p53 Homo sapiens 32-35 26696550-0 2016 TP53 Codon 72 Polymorphism Predicts Efficacy of Paclitaxel Plus Capecitabine Chemotherapy in Advanced Gastric Cancer Patients. Paclitaxel 48-58 tumor protein p53 Homo sapiens 0-4 26696550-1 2016 BACKGROUND AND AIMS: The present study analyzed the relationship between TP53 codon 72 polymorphisms and the clinical outcome of advanced gastric cancer patients receiving capecitabine plus paclitaxel chemotherapy. Paclitaxel 190-200 tumor protein p53 Homo sapiens 73-77 26696550-5 2016 RESULTS: The Pro/Pro genotypes of TP53 codon 72 were significantly correlated with a lower response rate to capecitabine plus paclitaxel chemotherapy in patients with gastric cancer when compared to the Arg/Arg genotype (30.6 vs. 63.2%, p value 0.000). Paclitaxel 126-136 tumor protein p53 Homo sapiens 34-38 26696550-7 2016 CONCLUSIONS: TP53 codon 72 polymorphisms was effective in predicting the response to chemotherapy and correlate with PFS and OS in patients with advanced gastric cancer treated with paclitaxel and capecitabine chemotherapy. Paclitaxel 182-192 tumor protein p53 Homo sapiens 13-17 26799187-0 2016 p38 MAPK-induced MDM2 degradation confers paclitaxel resistance through p53-mediated regulation of EGFR in human lung cancer cells. Paclitaxel 42-52 tumor protein p53 Homo sapiens 72-75 26799187-9 2016 These results suggest for the first time that the p38 MAPK/p53/EGFR axis is crucial for the facilitation of PTX resistance in NSCLCs. Paclitaxel 108-111 tumor protein p53 Homo sapiens 59-62 26799187-11 2016 These results provide a foundation for the future development of potential therapeutic strategies to regulate the p38 MAPK/p53/EGFR pathway for the treatment of lung cancer patients with PTX resistance. Paclitaxel 187-190 tumor protein p53 Homo sapiens 123-126 26773176-11 2016 In paclitaxel-resistant cells, there was a significant increase in Six1 and BCL-2 mRNA levels (p = 0.0007) with a marked decrease in pro-apoptotic Bax mRNA expression level (p = 0.03); however, there was no significant change in P53 expression (p = 0.025). Paclitaxel 3-13 tumor protein p53 Homo sapiens 229-232 26146988-7 2015 In addition, CDK5 knockdown alone and in combination with paclitaxel induced G1 cell cycle arrest and caspase 3 dependent apoptotic cell death associated with post-translational upregulation and nuclear translocation of TP53 and p27(Kip1) as well as TP53-dependent transcriptional induction of p21(Cip1) in wild type TP53 cancer cells. Paclitaxel 58-68 tumor protein p53 Homo sapiens 250-254 26177745-3 2015 Paclitaxel and other microtubule inhibitors can inhibit the growth of different types of cancer cells and induce apoptosis which is believed to be p53-independent. Paclitaxel 0-10 tumor protein p53 Homo sapiens 147-150 26146988-7 2015 In addition, CDK5 knockdown alone and in combination with paclitaxel induced G1 cell cycle arrest and caspase 3 dependent apoptotic cell death associated with post-translational upregulation and nuclear translocation of TP53 and p27(Kip1) as well as TP53-dependent transcriptional induction of p21(Cip1) in wild type TP53 cancer cells. Paclitaxel 58-68 tumor protein p53 Homo sapiens 250-254 26146988-7 2015 In addition, CDK5 knockdown alone and in combination with paclitaxel induced G1 cell cycle arrest and caspase 3 dependent apoptotic cell death associated with post-translational upregulation and nuclear translocation of TP53 and p27(Kip1) as well as TP53-dependent transcriptional induction of p21(Cip1) in wild type TP53 cancer cells. Paclitaxel 58-68 tumor protein p53 Homo sapiens 220-224 25647149-7 2015 Paclitaxel increased p53 protein expression in 10A, 10AT, 10ATG3B and 10CA1a cells, by 87, 102, 812 and 84%, respectively. Paclitaxel 0-10 tumor protein p53 Homo sapiens 21-24 25596561-1 2015 Paclitaxel is an alternative chemotherapeutic agent for chronic myelogenous leukemia (CML) when primary or secondary resistance of tyrosine kinase inhibitors (TKI) is emerging, because paclitaxel could bypass the apoptotic deficiencies linked to p53 and fas ligand pathways in CML. Paclitaxel 0-10 tumor protein p53 Homo sapiens 246-249 25780454-0 2015 Curcumin improves the paclitaxel-induced apoptosis of HPV-positive human cervical cancer cells via the NF-kappaB-p53-caspase-3 pathway. Paclitaxel 22-32 tumor protein p53 Homo sapiens 113-116 25780454-8 2015 The expression levels of p53 protein and cleaved caspase-3 were increased significantly in the curcumin plus paclitaxel-treated HeLa and CaSki cells compared with those in the cells treated with paclitaxel alone (P<0.01). Paclitaxel 109-119 tumor protein p53 Homo sapiens 25-28 25780454-8 2015 The expression levels of p53 protein and cleaved caspase-3 were increased significantly in the curcumin plus paclitaxel-treated HeLa and CaSki cells compared with those in the cells treated with paclitaxel alone (P<0.01). Paclitaxel 195-205 tumor protein p53 Homo sapiens 25-28 25780454-10 2015 This suggests that the combined effect of curcumin and paclitaxel was associated with the NF-kappaB-p53-caspase-3 pathway. Paclitaxel 55-65 tumor protein p53 Homo sapiens 100-103 25780454-11 2015 In conclusion, curcumin has the ability to improve the paclitaxel-induced apoptosis of HPV-positive human cervical cancer cell lines via the NF-kappaB-p53-caspase-3 pathway. Paclitaxel 55-65 tumor protein p53 Homo sapiens 151-154 25633416-9 2015 FOXM1 effector genes such as CDK4, p53 and cyclin D1 were downregulated in gastric cancer cells by combination treatment with DIM and paclitaxel. Paclitaxel 134-144 tumor protein p53 Homo sapiens 35-38 25647149-13 2015 The decreased responsiveness to paclitaxel observed in 10CA1a tumor cells was likely due, in part, to activation of the Akt signaling pathway and a high expression of wild-type p53 with lack of p21Waf1/Cip1. Paclitaxel 32-42 tumor protein p53 Homo sapiens 177-180 25411964-8 2014 FOXM1 knockdown significantly inhibited migration and invasion of ovarian cancer cells and enhanced paclitaxel-mediated cell death and mitotic catastrophe in a p53-independent manner. Paclitaxel 100-110 tumor protein p53 Homo sapiens 160-163 25499080-3 2015 Silencing of p53 or KRAS in A549 or H358 cells either enhanced or attenuated the resistance of cells to cisplatin and taxol through promotion or suppression of the NF-kappaB p65 nuclear translocation. Paclitaxel 118-123 tumor protein p53 Homo sapiens 13-16 25351378-0 2015 Biological characteristics of Taxol-resistant ovarian cancer cells and reversal of Taxol resistance by adenovirus expressing p53. Paclitaxel 83-88 tumor protein p53 Homo sapiens 125-128 25310526-7 2015 p53 and Bax were upregulated and Bcl2 was downregulated in the EB1-depleted PTX-treated MCF-7 cells, indicating that the apoptosis occurs via a p53-dependent pathway. Paclitaxel 76-79 tumor protein p53 Homo sapiens 0-3 25310526-7 2015 p53 and Bax were upregulated and Bcl2 was downregulated in the EB1-depleted PTX-treated MCF-7 cells, indicating that the apoptosis occurs via a p53-dependent pathway. Paclitaxel 76-79 tumor protein p53 Homo sapiens 144-147 25164962-4 2015 Sequential treatment of Taxol or cisplatin, followed by MK-2206, induced a synergistic inhibition of cell proliferation and effectively promoted cell death, either by inhibiting the phosphorylation of Akt and its downstream effectors 4E-BP1 and p70S6K in SKOV3 cells or by restoring p53 levels, which were downregulated after Taxol or cisplatin treatment, in ES2 cells. Paclitaxel 24-29 tumor protein p53 Homo sapiens 283-286 24189097-1 2014 For developing a multifunctional bioreducible targeted and synergistic co-delivery system for anticancer drug paclitaxel (PTX) and p53 gene for potential cancer therapy, supramolecular self-assembled inclusion complex was prepared from PTX and star-shaped cationic polymer containing gamma-cyclodextrin (gamma-CD) and multiple oligoethylenimine (OEI) arms with folic acid (FA) conjugated via a disulfide linker. Paclitaxel 236-239 tumor protein p53 Homo sapiens 131-134 25688502-13 2014 CONCLUSIONS: Irinotecan and paclitaxel are an effective treatment for HCT 116 wt cells, whereas HCT 116 cells with p53 deficiency can be treated successfully with paclitaxel and gemcitabine. Paclitaxel 163-173 tumor protein p53 Homo sapiens 115-118 24712391-5 2014 The improvements in therapeutic response over either PTX-VE or 5-FU-TPGS therapy alone were demonstrated by the ability to effectively induce the apoptosis of tumor cells via up-regulation of tumor suppressor p53 and beta-tubulin and by the significant inhibition of cell cycle progression. Paclitaxel 53-56 tumor protein p53 Homo sapiens 209-212 24787013-6 2014 EBV sensitized TP53-mutated BL cells to all spindle poisons tested, including vincristine and taxol, an effect that was systematically downmodulated by pretreatment of cells with inhibitors of p38 and c-Jun N-terminal kinase (JNK) mitogen-activated protein kinases. Paclitaxel 94-99 tumor protein p53 Homo sapiens 15-19 24565839-0 2014 p53 down-regulates SETDB1 gene expression during paclitaxel induced-cell death. Paclitaxel 49-59 tumor protein p53 Homo sapiens 0-3 24565839-5 2014 PTX treatment induces the p53 protein, but down-regulates expression of SETDB1 at the transcriptional level as well as the protein level. Paclitaxel 0-3 tumor protein p53 Homo sapiens 26-29 24565839-10 2014 This result demonstrates that PTX down-regulates SETDB1 gene expression in a p53 dependent manner, and p53 might participate in heterochromatic repression on the promoter regions of SETDB1. Paclitaxel 30-33 tumor protein p53 Homo sapiens 77-80 24189097-8 2014 Therefore, the multifunctional gamma-CD-OEI-SS-FA/PTX self-assembly system with the synergistic effects of redox-sensitive FA-targeted and PTX-enhanced p53 gene delivery may be promising for cancer therapeutic application. Paclitaxel 50-53 tumor protein p53 Homo sapiens 152-155 24189097-8 2014 Therefore, the multifunctional gamma-CD-OEI-SS-FA/PTX self-assembly system with the synergistic effects of redox-sensitive FA-targeted and PTX-enhanced p53 gene delivery may be promising for cancer therapeutic application. Paclitaxel 139-142 tumor protein p53 Homo sapiens 152-155 23161364-0 2013 p53 acetylation enhances Taxol-induced apoptosis in human cancer cells. Paclitaxel 25-30 tumor protein p53 Homo sapiens 0-3 24141649-11 2013 SNU-1528 had an in-frame deletion of 42 base pairs of p53 gene and showed over 20-fold resistance for taxol compared to the other cell lines. Paclitaxel 102-107 tumor protein p53 Homo sapiens 54-57 23735541-10 2013 Decrease of p53 and Bcl-2, fragmentation of DNA, increase of Bax and, finally, activation of caspases 3 and 9 in NB4 leukaemia cells make the apoptotic process induced by Ptx irreversible. Paclitaxel 171-174 tumor protein p53 Homo sapiens 12-15 23161364-5 2013 p53 was upregulated upon Taxol treatment in p53 wild type cells and deletion of p53 diminished Taxol-induced apoptosis. Paclitaxel 25-30 tumor protein p53 Homo sapiens 44-47 23161364-5 2013 p53 was upregulated upon Taxol treatment in p53 wild type cells and deletion of p53 diminished Taxol-induced apoptosis. Paclitaxel 25-30 tumor protein p53 Homo sapiens 44-47 23161364-5 2013 p53 was upregulated upon Taxol treatment in p53 wild type cells and deletion of p53 diminished Taxol-induced apoptosis. Paclitaxel 95-100 tumor protein p53 Homo sapiens 0-3 23161364-4 2013 Here we investigated the function of p53 in Taxol-induced apoptosis using p53 wild type and p53 null cancer cell lines. Paclitaxel 44-49 tumor protein p53 Homo sapiens 37-40 23161364-6 2013 p53 target proteins including MDM2, p21, BAX, and beta-isoform of PUMA were also upregulated by Taxol in p53 wild type cells. Paclitaxel 96-101 tumor protein p53 Homo sapiens 0-3 23161364-5 2013 p53 was upregulated upon Taxol treatment in p53 wild type cells and deletion of p53 diminished Taxol-induced apoptosis. Paclitaxel 25-30 tumor protein p53 Homo sapiens 0-3 23161364-6 2013 p53 target proteins including MDM2, p21, BAX, and beta-isoform of PUMA were also upregulated by Taxol in p53 wild type cells. Paclitaxel 96-101 tumor protein p53 Homo sapiens 105-108 23161364-7 2013 Conversely, when the wild type p53 was re-introduced into two different p53 null cancer cell lines, Taxol-induced apoptosis was enhanced. Paclitaxel 100-105 tumor protein p53 Homo sapiens 31-34 23023313-3 2012 In this study, we used MCF-7 and MDA-MB-231 human breast carcinoma cells which have different estrogen receptor (ER) and tumor suppressor p53 statuses to examine the mechanisms of taxol-induced growth inhibition and apoptosis. Paclitaxel 204-209 tumor protein p53 Homo sapiens 150-153 23161364-7 2013 Conversely, when the wild type p53 was re-introduced into two different p53 null cancer cell lines, Taxol-induced apoptosis was enhanced. Paclitaxel 100-105 tumor protein p53 Homo sapiens 72-75 23161364-8 2013 Among post-translational modifications that affect p53 stability and function, p53 acetylation, rather than phosphorylation, increased significantly in Taxol-treated cells. Paclitaxel 152-157 tumor protein p53 Homo sapiens 51-54 23161364-8 2013 Among post-translational modifications that affect p53 stability and function, p53 acetylation, rather than phosphorylation, increased significantly in Taxol-treated cells. Paclitaxel 152-157 tumor protein p53 Homo sapiens 79-82 23161364-9 2013 When acetylation was enhanced by anti-Sirt1 siRNA or an HDAC inhibitor, Taxol-induced apoptosis was enhanced, which was not observed in p53 null cells. Paclitaxel 72-77 tumor protein p53 Homo sapiens 136-139 23161364-11 2013 Thus, p53 plays a pro-apoptotic role in Taxol-induced apoptosis and acetylation of p53 contributes to this pro-apoptotic function in response to Taxol in several human cancer cell lines, suggesting that enhancing acetylation of p53 could have potential implication for increasing the sensitivity of cancer cells to Taxol. Paclitaxel 40-45 tumor protein p53 Homo sapiens 6-9 23161364-11 2013 Thus, p53 plays a pro-apoptotic role in Taxol-induced apoptosis and acetylation of p53 contributes to this pro-apoptotic function in response to Taxol in several human cancer cell lines, suggesting that enhancing acetylation of p53 could have potential implication for increasing the sensitivity of cancer cells to Taxol. Paclitaxel 145-150 tumor protein p53 Homo sapiens 83-86 23161364-11 2013 Thus, p53 plays a pro-apoptotic role in Taxol-induced apoptosis and acetylation of p53 contributes to this pro-apoptotic function in response to Taxol in several human cancer cell lines, suggesting that enhancing acetylation of p53 could have potential implication for increasing the sensitivity of cancer cells to Taxol. Paclitaxel 145-150 tumor protein p53 Homo sapiens 83-86 23161364-11 2013 Thus, p53 plays a pro-apoptotic role in Taxol-induced apoptosis and acetylation of p53 contributes to this pro-apoptotic function in response to Taxol in several human cancer cell lines, suggesting that enhancing acetylation of p53 could have potential implication for increasing the sensitivity of cancer cells to Taxol. Paclitaxel 145-150 tumor protein p53 Homo sapiens 83-86 23161364-11 2013 Thus, p53 plays a pro-apoptotic role in Taxol-induced apoptosis and acetylation of p53 contributes to this pro-apoptotic function in response to Taxol in several human cancer cell lines, suggesting that enhancing acetylation of p53 could have potential implication for increasing the sensitivity of cancer cells to Taxol. Paclitaxel 145-150 tumor protein p53 Homo sapiens 83-86 23534290-5 2013 Thus, in ATC cells the ionizing radiation and Ptx exhibited competitive effects upon phosphorylation of cell cycle controllers: p53, pRb, CHK2, cAbl and expression of Bax. Paclitaxel 46-49 tumor protein p53 Homo sapiens 128-131 24601052-6 2013 p53 positive expression and Ki67 high expression were associated with high PTX (p = 0.01 and p < 0.01, respectively) and CBDCA (p = 0.03 and p < 0.01, respectively) sensitivity. Paclitaxel 75-78 tumor protein p53 Homo sapiens 0-3 24381593-3 2013 We hypothesized that synthetic lethality can be achieved in endometrial cancer cells with mutant p53 by combining paclitaxel with agents to overcome G2/M arrest and induce mitotic catastrophe. Paclitaxel 114-124 tumor protein p53 Homo sapiens 97-100 24381593-4 2013 The combination of BIBF1120, an investigational VEGFR, PDGFR, and FGFR multityrosine kinase inhibitor with established anti-angiogenic activity, with paclitaxel abrogated the G2/M checkpoint in p53-null endometrial cancer cells via modulation of G2/M checkpoint regulators followed by induction of mitotic cell death. Paclitaxel 150-160 tumor protein p53 Homo sapiens 194-197 24381593-5 2013 In endometrial cancer cells harboring an oncogenic gain-of-function p53 mutation, synthetic lethality was created by combining paclitaxel with BIBF1120 and a histone deacetylase inhibitor, which serves to destabilize mutant p53. Paclitaxel 127-137 tumor protein p53 Homo sapiens 68-71 24381593-5 2013 In endometrial cancer cells harboring an oncogenic gain-of-function p53 mutation, synthetic lethality was created by combining paclitaxel with BIBF1120 and a histone deacetylase inhibitor, which serves to destabilize mutant p53. Paclitaxel 127-137 tumor protein p53 Homo sapiens 224-227 22885806-1 2012 We have examined the relationship between chemotherapy-induced mitotic catastrophe and cell death by apoptosis in both wild-type and p53(-/-) HCT116 human colon carcinoma cells treated with nanomolar concentrations of paclitaxel (PTX), a drug that acts on tubulin altering the normal development of mitosis. Paclitaxel 218-228 tumor protein p53 Homo sapiens 133-136 22885806-3 2012 In the presence of PTX, the percentage of polyploid cells observed was higher in p53-deficient cells, indicating that mitotic slippage was favored compared to wild-type cells, with the presence of large multinucleate cells. Paclitaxel 19-22 tumor protein p53 Homo sapiens 81-84 22885806-5 2012 Lack of p53 facilitated endoreduplication and polyploidy in PTX-treated cells, but cells were still killed with similar efficacy through the same apoptotic-like mechanism in the absence of caspase activity. Paclitaxel 60-63 tumor protein p53 Homo sapiens 8-11 23023313-9 2012 These findings suggest that taxol-induced G2/M arrest and apoptosis in human breast carcinoma cells is mediated through the ER- and p53-independent upregulation of p21. Paclitaxel 40-45 tumor protein p53 Homo sapiens 156-159 21926165-4 2011 Changes in proliferation, mitotic catastrophe, apoptosis, and underlying mechanism in ovarian cancer cells of different p53 status following paclitaxel exposure were also analyzed. Paclitaxel 141-151 tumor protein p53 Homo sapiens 120-123 22549660-6 2012 Our findings indicated that by synergism with anticancer drugs, FLX modulation of apoptosis via targeting p53 and Bcl-2 expression, FLX reverse the breast cancer cell"s resistance and enhance the chemosensitivity to ADM and PTX. Paclitaxel 224-227 tumor protein p53 Homo sapiens 106-109 22534478-4 2012 RESULTS: p53 expression were associated with the significantly shorter disease-free survival (DFS) (p<0.001) and overall survival (OS) (p=0.012) in the curatively resected advanced gastric cancer patients receiving capecitabine plus paclitaxel. Paclitaxel 236-246 tumor protein p53 Homo sapiens 9-12 22534478-6 2012 CONCLUSIONS: p53 expression positive might predict prognosis in gastric cancer patients who underwent curative surgery followed by adjuvant capecitabine plus paclitaxel chemotherapy. Paclitaxel 158-168 tumor protein p53 Homo sapiens 13-16 22534478-7 2012 A favorable effect of capecitabine plus paclitaxel might therefore be expected in patients that do not express p53. Paclitaxel 40-50 tumor protein p53 Homo sapiens 111-114 22077725-3 2011 We have examined potential alterations in p53 in response to 2-ME(2), E(2) and the microtubule disruptor taxol in T47D breast cancer cells. Paclitaxel 105-110 tumor protein p53 Homo sapiens 42-45 22077725-8 2011 The observed upregulation of p53 induced by 2-ME(2) is inhibited by concurrent treatment with 1 microM taxol. Paclitaxel 103-108 tumor protein p53 Homo sapiens 29-32 22765290-3 2012 In this review, we focus on highlighting several representative plant natural compounds such as curcumin, resveratrol, paclitaxel, oridonin, quercetin and plant lectin - that may lead to cancer cell death - for regulation of some core autophagic pathways, involved in Ras-Raf signalling, Beclin-1 interactome, BCR-ABL, PI3KCI/Akt/mTOR, FOXO1 signalling and p53. Paclitaxel 119-129 tumor protein p53 Homo sapiens 357-360 22489661-0 2012 Radiation/paclitaxel treatment of p53-abnormal non-small cell lung cancer xenograft tumor and associated mechanism. Paclitaxel 10-20 tumor protein p53 Homo sapiens 34-37 22493354-1 2012 BACKGROUND/AIM: This study specifies a strategy to improve radiotherapy by partial synchronization of p53-deficient cancer cells (FaDu and H1299) in mitosis using taxol, with protecting p53 wild-type cells (A549) by the prior administration of cytostatic compounds. Paclitaxel 163-168 tumor protein p53 Homo sapiens 102-105 20624405-1 2010 AIMS: the aims of the study are to investigate the additive effect of exogenous short-carbon chain phospholipids, C(2)-ceramide, on an anti-cancer drug paclitaxel (PTX)-induced senescence of human non-small cell lung cancer (NSCLC) cells deficient in functional p53 and p16, and to examine whether mitogen-activated protein kinase (MAPK) plays a role in ceramide-sensitized senescence of NSCLC cells. Paclitaxel 152-162 tumor protein p53 Homo sapiens 262-265 21594648-8 2011 Importantly, miR-22 overexpression enhanced the cytotoxic role of paclitaxel in p53-mutated HT-29 and HCT-15 cells, but not in p53 wild-type HCT-116 cell. Paclitaxel 66-76 tumor protein p53 Homo sapiens 80-83 21514041-0 2011 Gene expression signature of TP53 but not its mutation status predicts response to sequential paclitaxel and 5-FU/epirubicin/cyclophosphamide in human breast cancer. Paclitaxel 94-104 tumor protein p53 Homo sapiens 29-33 21514041-1 2011 PURPOSE: The aim of this study was to determine whether TP53 mutation status (MS) can predict response of breast cancer to paclitaxel followed by 5-FU/epirubicin/cyclophosphamide (P-FEC). Paclitaxel 123-133 tumor protein p53 Homo sapiens 56-60 21482024-7 2011 Ki23057 increased the p53 expression level in OCUM-2M/SN38 and OCUM-2M/PTX, but not in OCUM-2M/VP16. Paclitaxel 71-74 tumor protein p53 Homo sapiens 22-25 21693655-3 2011 PATIENTS AND METHODS: Epithelial p53 expression was evaluated using two immunohistochemical antibodies (DO7 and 1801) in formalin-fixed, paraffin-embedded tissue from patients with node-positive breast cancer who were randomized to four cycles of cyclophosphamide and one of three doses of doxorubicin (60, 75, or 90 mg/m(2); AC) and to receive four subsequent cycles of paclitaxel (T) or not. Paclitaxel 371-381 tumor protein p53 Homo sapiens 33-36 21693655-9 2011 CONCLUSION: Nuclear staining of p53 by immunohistochemistry is associated with worse prognosis in node-positive patients treated with adjuvant doxorubicin-based chemotherapy but is not a useful predictor of benefit from doxorubicin dose escalation or the addition of paclitaxel. Paclitaxel 267-277 tumor protein p53 Homo sapiens 32-35 21556366-0 2011 Predictive and prognostic impact of TP53 mutations and MDM2 promoter genotype in primary breast cancer patients treated with epirubicin or paclitaxel. Paclitaxel 139-149 tumor protein p53 Homo sapiens 36-40 21556366-10 2011 Remarkably, TP53 mutations (p = 0.007) but also MDM2 309TG/GG genotype status (p = 0.012) were associated with a poor disease-specific survival among patients having paclitaxel but not patients having epirubicin first-line. Paclitaxel 166-176 tumor protein p53 Homo sapiens 12-16 21556366-13 2011 In contrast, TP53 mutations and MDM2 309G allele status conferred poor disease-specific survival among patients treated with primary paclitaxel but not epirubicin monotherapy. Paclitaxel 133-143 tumor protein p53 Homo sapiens 13-17 21109480-8 2011 In combination therapy, p53RA small molecules enhanced the anti-tumor activity of cisplatin, 5-fluorouracil, paclitaxel, and erlotinib against HNSCC cells. Paclitaxel 109-119 tumor protein p53 Homo sapiens 24-27 20878066-0 2010 Amifostine enhancement of the anti-cancer effects of paclitaxel in endometrial cancer is TP53-dependent. Paclitaxel 53-63 tumor protein p53 Homo sapiens 89-93 20878066-5 2010 In this report, using a cell line with knock-down p53 expression through siRNA, we found that amifostine enhancement of paclitaxel"s anticancer effect is p53 status-dependent. Paclitaxel 120-130 tumor protein p53 Homo sapiens 50-53 20878066-5 2010 In this report, using a cell line with knock-down p53 expression through siRNA, we found that amifostine enhancement of paclitaxel"s anticancer effect is p53 status-dependent. Paclitaxel 120-130 tumor protein p53 Homo sapiens 154-157 20878066-8 2010 Sensitivity to the therapeutic effect of paclitaxel in combination with amifostine was dependent upon the status of p53. Paclitaxel 41-51 tumor protein p53 Homo sapiens 116-119 20878066-9 2010 A tumor with a nonsense TP53 mutation showed increased therapeutic response to paclitaxel and amifostine as measured by tumor weight compared to a tumor with wild- type TP53. Paclitaxel 79-89 tumor protein p53 Homo sapiens 24-28 20878066-10 2010 Our study provides a rationale for a clinical trial of combined paclitaxel and amifostine in endometrial cancer patients whose tumors harbor TP53 mutations. Paclitaxel 64-74 tumor protein p53 Homo sapiens 141-145 21594648-0 2011 Overexpression of miR-22 reverses paclitaxel-induced chemoresistance through activation of PTEN signaling in p53-mutated colon cancer cells. Paclitaxel 34-44 tumor protein p53 Homo sapiens 109-112 21594648-4 2011 We further investigated the role of miR-22 on cytotoxicity of paclitaxel in both the p53-mutated and p53 wild-type colon cancer cells. Paclitaxel 62-72 tumor protein p53 Homo sapiens 101-104 21354697-3 2011 Importantly, miR-203 overexpression increased the cytotoxic role of paclitaxel in the p53-mutated colon cancer cells, but not in the p53 wild-type cells. Paclitaxel 68-78 tumor protein p53 Homo sapiens 86-89 22194993-3 2011 In the present study we investigated the effect of paclitaxel in combination with two novel HDACi, ST2782 or ST3595, able to induce p53 and tubulin hyperacetylation. Paclitaxel 51-61 tumor protein p53 Homo sapiens 132-135 22194993-4 2011 A synergistic effect of the paclitaxel/ST2782 (or ST3595) combination was found in wild-type p53 ovarian carcinoma cells, but not in a p53 mutant subline, in spite of a marked tubulin acetylation. Paclitaxel 28-38 tumor protein p53 Homo sapiens 93-96 22194993-9 2011 Our results support the relevance of p53 modulation as a major determinant of the synergistic interaction observed between paclitaxel and novel HDACi and emphasize the therapeutic interest of this combination. Paclitaxel 123-133 tumor protein p53 Homo sapiens 37-40 20624405-1 2010 AIMS: the aims of the study are to investigate the additive effect of exogenous short-carbon chain phospholipids, C(2)-ceramide, on an anti-cancer drug paclitaxel (PTX)-induced senescence of human non-small cell lung cancer (NSCLC) cells deficient in functional p53 and p16, and to examine whether mitogen-activated protein kinase (MAPK) plays a role in ceramide-sensitized senescence of NSCLC cells. Paclitaxel 164-167 tumor protein p53 Homo sapiens 262-265 19363466-11 2009 The growth of SiHa xenograft tumors was reduced using paclitaxel combined with intronic and exonic siRNA, compared with exonic siRNA alone, confirming the synergistic relationship between p53 restoration and paclitaxel. Paclitaxel 54-64 tumor protein p53 Homo sapiens 188-191 20178585-0 2010 Protection of p53 wild type cells from taxol by nutlin-3 in the combined lung cancer treatment. Paclitaxel 39-44 tumor protein p53 Homo sapiens 14-17 19918798-5 2010 PTX/LPC combination acted by favoring p53 stabilization through a lowering in p-Akt levels and in ps166-MDM2, the phosphorylated-MDM2 form that enters the nucleus and induces p53 export and degradation. Paclitaxel 0-3 tumor protein p53 Homo sapiens 38-41 19918798-5 2010 PTX/LPC combination acted by favoring p53 stabilization through a lowering in p-Akt levels and in ps166-MDM2, the phosphorylated-MDM2 form that enters the nucleus and induces p53 export and degradation. Paclitaxel 0-3 tumor protein p53 Homo sapiens 175-178 19918798-8 2010 PTX/LPC treatment induced a weakness of Akt-MDM2-p53 complex and increased nuclear p53 levels. Paclitaxel 0-3 tumor protein p53 Homo sapiens 49-52 19918798-8 2010 PTX/LPC treatment induced a weakness of Akt-MDM2-p53 complex and increased nuclear p53 levels. Paclitaxel 0-3 tumor protein p53 Homo sapiens 83-86 19815708-6 2009 Here, we show that sirolimus and paclitaxel differentially induce self-digesting autophagy in vascular endothelial cells with changes in expression of LC3B, p53, and Bcl-2, considerably suppressing re-endothelialization and revascularization. Paclitaxel 33-43 tumor protein p53 Homo sapiens 157-160 20944137-0 2010 Increasing p53 protein sensitizes non-small cell lung cancer to paclitaxel and cisplatin in vitro. Paclitaxel 64-74 tumor protein p53 Homo sapiens 11-14 20944137-7 2010 A significant positive correlation between p53 protein concentration and cytotoxic response was demonstrated (R(2) for CDDP=0.823; R(2) for PAX=0.909; p<0.001). Paclitaxel 140-143 tumor protein p53 Homo sapiens 43-46 20944137-8 2010 CONCLUSION: Increasing intracellular p53 protein concentrations can augment the effect of CDDP and PAX in NSCLC, despite the baseline level of p53 protein expression. Paclitaxel 99-102 tumor protein p53 Homo sapiens 37-40 20661829-0 2010 Protection of p53 wild type cells from taxol by genistein in the combined treatment of lung cancer. Paclitaxel 39-44 tumor protein p53 Homo sapiens 14-17 20661829-1 2010 This study specifies the basic principles to selectively kill p53-deficient cells (H1299, FaDu) by taxol and to protect p53 wild type cells (A549) by the prior administration of structurally related flavonoids (apigenin, genistein, and quercetin). Paclitaxel 99-104 tumor protein p53 Homo sapiens 62-65 20661829-7 2010 The proposed therapeutic strategy allows protection of p53 wild type cells from taxol and selectively increases apoptosis in p53-deficient cells. Paclitaxel 80-85 tumor protein p53 Homo sapiens 55-58 20661829-7 2010 The proposed therapeutic strategy allows protection of p53 wild type cells from taxol and selectively increases apoptosis in p53-deficient cells. Paclitaxel 80-85 tumor protein p53 Homo sapiens 125-128 19000447-10 2008 The strong expression of p53 was correlated with decreased inhibition rates of PTX and DDP on cancer cells (P<0.05, P<0.01). Paclitaxel 79-82 tumor protein p53 Homo sapiens 25-28 19052714-0 2009 TP53 codon 72 polymorphism associated with prognosis in patients with advanced gastric cancer treated with paclitaxel and cisplatin. Paclitaxel 107-117 tumor protein p53 Homo sapiens 0-4 19052714-6 2009 CONCLUSION: The TP53 codon 72 SNP was found to be predictive of the response to chemotherapy and correlate with the time to progression in patients with advanced gastric cancer treated with paclitaxel and cisplatin chemotherapy. Paclitaxel 190-200 tumor protein p53 Homo sapiens 16-20 18758183-2 2009 P27 and P53 play important roles in the signal transduction leading to neointimal growth inhibition and induction of apoptosis of smooth muscle cells due to rapamycin and paclitaxel. Paclitaxel 171-181 tumor protein p53 Homo sapiens 8-11 19421315-6 2009 We used the microtubules damaging agent paclitaxel (PTX), to arrest the cells in the M phase, in a p53 mutated melanoma cell line with modulated Myc level and activity. Paclitaxel 40-50 tumor protein p53 Homo sapiens 99-102 19421315-6 2009 We used the microtubules damaging agent paclitaxel (PTX), to arrest the cells in the M phase, in a p53 mutated melanoma cell line with modulated Myc level and activity. Paclitaxel 52-55 tumor protein p53 Homo sapiens 99-102 19217709-0 2009 Role of p53 in the induction of cyclooxygenase-2 by cisplatin or paclitaxel in non-small cell lung cancer cell lines. Paclitaxel 65-75 tumor protein p53 Homo sapiens 8-11 19217709-10 2009 For paclitaxel treatment, an increase in COX-2 mRNA expression was observed in H460 and A549 (wild-type p53 cell lines). Paclitaxel 4-14 tumor protein p53 Homo sapiens 104-107 19217709-11 2009 Moreover, paclitaxel treatment increased COX-2 expression in ACC-LC-319 cell lines (p53 null), showing a p53-independent effect. Paclitaxel 10-20 tumor protein p53 Homo sapiens 84-87 19217709-11 2009 Moreover, paclitaxel treatment increased COX-2 expression in ACC-LC-319 cell lines (p53 null), showing a p53-independent effect. Paclitaxel 10-20 tumor protein p53 Homo sapiens 105-108 19397590-5 2009 Flow cytometry and fluorescence microscopy revealed that although As(2)O(3) alone caused a moderate level of mitotic arrest, it greatly attenuated paclitaxel-induced mitotic arrest in cells with p53 deficiency. Paclitaxel 147-157 tumor protein p53 Homo sapiens 195-198 19332559-3 2009 p53 has long been known to be activated by spindle poisons, such as nocodazole and Taxol, although the underlying mechanism remains elusive. Paclitaxel 83-88 tumor protein p53 Homo sapiens 0-3 19148534-7 2009 Thus, TACC3 is thought to be the critical molecule in mediating the anticancer mechanisms of paclitaxel in p53 inactivated cells by inducing G2/M arrest and apoptosis. Paclitaxel 93-103 tumor protein p53 Homo sapiens 107-110 17823933-0 2007 Paclitaxel enhanced radiation sensitization for the suppression of human prostate cancer tumor growth via a p53 independent pathway. Paclitaxel 0-10 tumor protein p53 Homo sapiens 108-111 18158619-8 2008 Taken together, we present a molecular mechanism where Id-1 regulates p53 and NF-kappaB pathways, which in turn regulates Bax and Bcl-2 genes, thus providing a survival advantage under exogenous stress such as serum-free or taxol treatment in MCF-7 breast cancer cells. Paclitaxel 224-229 tumor protein p53 Homo sapiens 70-73 18806740-3 2008 RESULTS: Low dose of Taxol that cause apoptosis (25 nM) enhanced Rb protein phosphorylation, decreased the expression of cyclin-dependent kinase inhibitors p27(KIP1) and p21(WAF1) , and potentiated the accumulation of phosphorylated p53 and of the prolyl isomerase Pin1. Paclitaxel 21-26 tumor protein p53 Homo sapiens 233-236 18555006-4 2008 Furthermore, endogenous expression of p19(ras) and p73beta is significantly increased by Taxol treatment, and Taxol-enhanced endogenous p73beta transcriptional activities are further amplified by p19(ras), which markedly increased cellular apoptosis in p53-null SAOS2 cancer cell line. Paclitaxel 110-115 tumor protein p53 Homo sapiens 253-256 17960385-0 2008 The effect of p53 gene expression on the inhibition of cell proliferation by paclitaxel. Paclitaxel 77-87 tumor protein p53 Homo sapiens 14-17 17960385-1 2008 BACKGROUND/AIMS: We evaluated the relationship between p53 status and paclitaxel (PTX)-induced inhibition of the growth of human stomach cancer cells. Paclitaxel 70-80 tumor protein p53 Homo sapiens 55-58 17960385-1 2008 BACKGROUND/AIMS: We evaluated the relationship between p53 status and paclitaxel (PTX)-induced inhibition of the growth of human stomach cancer cells. Paclitaxel 82-85 tumor protein p53 Homo sapiens 55-58 17960385-11 2008 CONCLUSION: Both p53 status and cyclin-B1 expression might be useful for predicting the therapeutic response of stomach cancer to PTX. Paclitaxel 130-133 tumor protein p53 Homo sapiens 17-20 18516295-2 2008 We have previously shown that mutational inactivation of p53 results in sensitization to paclitaxel. Paclitaxel 89-99 tumor protein p53 Homo sapiens 57-60 18516295-7 2008 Sensitization to paclitaxel-induced apoptosis was also achieved by p53-siRNA transfection in wild type p53 H460 cells. Paclitaxel 17-27 tumor protein p53 Homo sapiens 67-70 18516295-7 2008 Sensitization to paclitaxel-induced apoptosis was also achieved by p53-siRNA transfection in wild type p53 H460 cells. Paclitaxel 17-27 tumor protein p53 Homo sapiens 103-106 18971636-11 2008 This regulation is observed in a transgenic p53-inducible cell system as well as in cells with wild-type p53 treated with nutlin-3, doxorubicin or paclitaxel. Paclitaxel 147-157 tumor protein p53 Homo sapiens 44-47 18813780-7 2008 Consistently, PTX increased p21WAF1, bax and MDM2 levels, suggesting that p53 is transcriptionally active. Paclitaxel 14-17 tumor protein p53 Homo sapiens 74-77 18469851-0 2008 Mechanism of G1-like arrest by low concentrations of paclitaxel: next cell cycle p53-dependent arrest with sub G1 DNA content mediated by prolonged mitosis. Paclitaxel 53-63 tumor protein p53 Homo sapiens 81-84 18469851-10 2008 We conclude that PTX directly affects cells only in mitosis and the duration of mitosis determines cell fate, including p53-dependent G1-like arrest. Paclitaxel 17-20 tumor protein p53 Homo sapiens 120-123 20731894-14 2008 pEGFP-p53(RS)-801D cell line showed a notably smaller value of IC50(2.34+/-0.43 ng/mL) to Paclitaxel(TAX) than 801D(8.40+/-1.50 ng/mL, P <0.05)did. Paclitaxel 90-100 tumor protein p53 Homo sapiens 6-9 18506998-11 2008 Immunohistochemical staining showed increased expression of p65 after paclitaxel treatment, while paclitaxel in combination with AdIkappaBalpha intratumoral injection eliminated this expression accompanied by the slightly reduced expression of VEGF, with stable p53 status. Paclitaxel 98-108 tumor protein p53 Homo sapiens 262-265 18319335-6 2008 One of these ATFs, 3ZF-1-VP, promoted paclitaxel resistance in cell lines having mutated or inactivated p53, such as MDA-MB-435 and Kaposi"s sarcoma cell lines. Paclitaxel 38-48 tumor protein p53 Homo sapiens 104-107 18205918-8 2008 We further found stronger correlations of bFGF level and paclitaxel sensitivity in four tumor subgroups (high stage, positive p53 staining, negative aFGF staining, containing higher-than-median bFGF level), compared to all other groups. Paclitaxel 57-67 tumor protein p53 Homo sapiens 126-129 18231754-11 2007 Moreover, p38MAPK-mediated apoptosis in paclitaxel-resistant ovarian carcinoma cells depends on the activation of p53. Paclitaxel 40-50 tumor protein p53 Homo sapiens 114-117 17823933-1 2007 BACKGROUND: This study investigated the influence of p53 status on treatment using combined paclitaxel and irradiation for human prostate cancer (PC) in vitro and in vivo. Paclitaxel 92-102 tumor protein p53 Homo sapiens 53-56 17823933-2 2007 METHODS: Enhancement of the radiation response by paclitaxel was determined by MTT and clonogenic assays in four sublines of the human PC cell line, LNCaP, stably transfected to express different p53 mutations found in PC patients. Paclitaxel 50-60 tumor protein p53 Homo sapiens 196-199 17823933-5 2007 RESULTS: Paclitaxel (8-10 nM) suppressed cell proliferation by 50% by inducing G2M mitotic arrest in LNCaP cell lines transfected to overexpress wild-type or mutant p53. Paclitaxel 9-19 tumor protein p53 Homo sapiens 165-168 17823933-10 2007 CONCLUSIONS: Pre-treatment with paclitaxel enhances radiation efficacy on cell killing and suppression of growth of human PC cell lines in vitro and in vivo via p53 independent pathways. Paclitaxel 32-42 tumor protein p53 Homo sapiens 161-164 17823933-11 2007 Paclitaxel has potential for use as a radiosensitizer in the treatment of patients with PC with either wild-type or mutant p53 genetic status. Paclitaxel 0-10 tumor protein p53 Homo sapiens 123-126 17912033-1 2007 We previously reported that the Polo-like Kinase 2 gene (Plk2/Snk) is a direct target for transcriptional regulation by p53 and that silencing Plk2 sensitizes cancer cells to Taxol-induced apoptosis. Paclitaxel 175-180 tumor protein p53 Homo sapiens 120-123 17636258-5 2007 Topotecan- and paclitaxel-resistant prostate cancer lines were as sensitive to p53p-Ant-induced targeted necrosis as parental lines. Paclitaxel 15-25 tumor protein p53 Homo sapiens 79-83 16459017-0 2006 Prognostic significance of p53 mutation in suboptimally resected advanced ovarian carcinoma treated with the combination chemotherapy of paclitaxel and carboplatin. Paclitaxel 137-147 tumor protein p53 Homo sapiens 27-30 17166391-4 2006 For example, paclitaxel is regarded as a relatively sensitive drug and may be chosen for the tumors with high expression of p53, while it is predicted as relatively resistant drug and should be avoided for the tumors with high expression of P-glycoprotein (P-gp). Paclitaxel 13-23 tumor protein p53 Homo sapiens 124-127 17686239-12 2007 CONCLUSION: Residual tumor, p53, and Pgp expression are predictive factors for the response to platinum/paclitaxel first-line adjuvant chemotherapy in advanced ovarian cancer. Paclitaxel 104-114 tumor protein p53 Homo sapiens 28-31 17244262-5 2007 Paclitaxel treatment combined with apoptin expression significantly inhibited the survival of p53-positive human osteosarcoma U2OS and non-small lung carcinoma A549 cells, p53-negative human osteosarcoma Saos-2 cells and p53-mutant human prostate cancer Du145 cells, already at low doses of the chemotherapeutic agent. Paclitaxel 0-10 tumor protein p53 Homo sapiens 94-97 17244262-5 2007 Paclitaxel treatment combined with apoptin expression significantly inhibited the survival of p53-positive human osteosarcoma U2OS and non-small lung carcinoma A549 cells, p53-negative human osteosarcoma Saos-2 cells and p53-mutant human prostate cancer Du145 cells, already at low doses of the chemotherapeutic agent. Paclitaxel 0-10 tumor protein p53 Homo sapiens 172-175 17244262-5 2007 Paclitaxel treatment combined with apoptin expression significantly inhibited the survival of p53-positive human osteosarcoma U2OS and non-small lung carcinoma A549 cells, p53-negative human osteosarcoma Saos-2 cells and p53-mutant human prostate cancer Du145 cells, already at low doses of the chemotherapeutic agent. Paclitaxel 0-10 tumor protein p53 Homo sapiens 172-175 16820892-7 2006 Gemcitabine and paclitaxel are highly efficient in the induction of apoptosis in ovarian cancer cells, which express a particular subset of the growth suppressor protein p53. Paclitaxel 16-26 tumor protein p53 Homo sapiens 170-173 16739339-0 2006 P53 gene status in patients with advanced serous epithelial ovarian cancer in relation to response to paclitaxel- plus platinum-based chemotherapy and long-term clinical outcome. Paclitaxel 102-112 tumor protein p53 Homo sapiens 0-3 15990222-0 2006 Induction of p53 and drug resistance following treatment with cisplatin or paclitaxel in ovarian cancer cell lines. Paclitaxel 75-85 tumor protein p53 Homo sapiens 13-16 15990222-3 2006 Cells (UL-3A, UL-3B) that recovered from cisplatin (Cis) and paclitaxel (Tax) treatments showed higher levels of p53, mdr-1 and chemoresistance than untreated controls. Paclitaxel 61-71 tumor protein p53 Homo sapiens 113-116 16687915-4 2006 If a cell stays in mitosis too long, (e.g. mitotic arrest caused by Taxol or nocodazole), then p53 accumulates. Paclitaxel 68-73 tumor protein p53 Homo sapiens 95-98 16364249-0 2006 TP53 and P21 polymorphisms: response to cisplatinum/paclitaxel-based chemotherapy in ovarian cancer. Paclitaxel 52-62 tumor protein p53 Homo sapiens 0-4 16356831-7 2006 Lower doses of 2-ME and paclitaxel resulted in G1 (but not G2/M) cell cycle arrest in the p53 wild type LNCaP cell line, but with minimal induction of apoptosis. Paclitaxel 24-34 tumor protein p53 Homo sapiens 90-93 16616141-0 2006 Evidence that low doses of Taxol enhance the functional transactivatory properties of p53 on p21 waf promoter in MCF-7 breast cancer cells. Paclitaxel 27-32 tumor protein p53 Homo sapiens 86-89 16616141-1 2006 In the present study, we evidence how in breast cancer cells low doses of Taxol for 18 h determined the upregulation of p53 and p21 waf expression concomitantly with a decrease of the anti-apoptotic Bcl-2. Paclitaxel 74-79 tumor protein p53 Homo sapiens 120-123 16616141-3 2006 Indeed, the most important finding of this study consists with the evidence that Taxol at lower concentrations is able to produce the activation of p21 promoter via p53. Paclitaxel 81-86 tumor protein p53 Homo sapiens 165-168 16739339-1 2006 BACKGROUND: The aim of this retrospective study was to assess whether p53 gene status has any predictive or prognostic relevance in patients with advanced, poorly-differentiated serous epithelial ovarian cancer treated with paclitaxel- plus platinum-based chemotherapy. Paclitaxel 224-234 tumor protein p53 Homo sapiens 70-73 15908516-6 2005 When treatment with E6 siRNA was coupled with chemotherapy, the p53 activity after treatment with carboplatin and paclitaxel was additively increased, whereas the p53 activation induced by the rest of the drugs was synergistically increased. Paclitaxel 114-124 tumor protein p53 Homo sapiens 64-67 15657900-6 2005 Co-exposure to C75 and Taxol induced a remarkable nuclear accumulation of activated p38 mitogen-activated protein kinase (p38 MAPK), which was accompanied by a synergistic nuclear accumulation of the p53 tumor-suppressor protein that was phosphorylated at Ser46, a p38 MAPK-regulated pro-apoptotic modification of p53. Paclitaxel 23-28 tumor protein p53 Homo sapiens 200-203 15870870-0 2005 Apoptosis induced by 5-fluorouracil, cisplatin and paclitaxel are associated with p53 gene status in gastric cancer cell lines. Paclitaxel 51-61 tumor protein p53 Homo sapiens 82-85 15870870-5 2005 From these results, our previous study suggests that cells with mutant-type p53 may be less responsive to FP treatment and the present study indicates that another anti-cancer drug like paclitaxel, which might be mediated by a p53-independent pathway, should be selected. Paclitaxel 186-196 tumor protein p53 Homo sapiens 76-79 15870870-5 2005 From these results, our previous study suggests that cells with mutant-type p53 may be less responsive to FP treatment and the present study indicates that another anti-cancer drug like paclitaxel, which might be mediated by a p53-independent pathway, should be selected. Paclitaxel 186-196 tumor protein p53 Homo sapiens 227-230 15863265-1 2005 In this study, we analyzed the role of the p53 status for paclitaxel/Taxol sensitivity in renal cell carcinomas (RCCs) of the clear cell type. Paclitaxel 58-68 tumor protein p53 Homo sapiens 43-46 15863265-1 2005 In this study, we analyzed the role of the p53 status for paclitaxel/Taxol sensitivity in renal cell carcinomas (RCCs) of the clear cell type. Paclitaxel 69-74 tumor protein p53 Homo sapiens 43-46 15657900-6 2005 Co-exposure to C75 and Taxol induced a remarkable nuclear accumulation of activated p38 mitogen-activated protein kinase (p38 MAPK), which was accompanied by a synergistic nuclear accumulation of the p53 tumor-suppressor protein that was phosphorylated at Ser46, a p38 MAPK-regulated pro-apoptotic modification of p53. Paclitaxel 23-28 tumor protein p53 Homo sapiens 314-317 15746064-4 2005 Here we have investigated the effect of combined treatment with ionizing radiation and patupilone or paclitaxel in the P-glycoprotein-overexpressing, p53-mutated human colon adenocarcinoma cell line SW480 and in murine, genetically defined E1A/ras-transformed paclitaxel-sensitive embryo fibroblasts. Paclitaxel 101-111 tumor protein p53 Homo sapiens 150-153 15711598-7 2005 Paclitaxel impairs microtubule function, causes G2/M cell cycle blockade, mitochondria damage, and p53-independent apoptosis. Paclitaxel 0-10 tumor protein p53 Homo sapiens 99-102 15691646-1 2005 We measured the expression of the p53 nuclear protein and epidermal growth factor receptor (EGFR) in 46 biopsy samples from patients with advanced head and neck cancer treated with induction combination chemotherapy of 5-fluorouracil, cisplatin, and paclitaxel. Paclitaxel 250-260 tumor protein p53 Homo sapiens 34-37 15592521-10 2005 Strikingly, CYR61 overexpression impaired the accumulation of wild-type p53 following Taxol exposure, while inhibition of alphavbeta3 or ERK1/ERK2 MAPK signalings completely restored Taxol-induced upregulation of p53. Paclitaxel 86-91 tumor protein p53 Homo sapiens 72-75 15592521-10 2005 Strikingly, CYR61 overexpression impaired the accumulation of wild-type p53 following Taxol exposure, while inhibition of alphavbeta3 or ERK1/ERK2 MAPK signalings completely restored Taxol-induced upregulation of p53. Paclitaxel 183-188 tumor protein p53 Homo sapiens 213-216 16122187-1 2005 PURPOSE: In this study the relationship between therapy with paclitaxel, cisplatin, vinorelbine and titanocene dichloride and of the expression of proliferation markers (ki67 and S-phase fraction) and tumour suppressor gene p53 was analyzed using a human ovarian cancer xenograft model. Paclitaxel 61-71 tumor protein p53 Homo sapiens 224-227 15662138-0 2005 The tumor suppressor p33ING1b enhances taxol-induced apoptosis by p53-dependent pathway in human osteosarcoma U2OS cells. Paclitaxel 39-44 tumor protein p53 Homo sapiens 66-69 15662138-4 2005 The results showed that p33ING1b markedly increased taxol-induced growth inhibition and apoptosis in p53+/+ U2OS cells, but not in p53-mutant MG63 cells. Paclitaxel 52-57 tumor protein p53 Homo sapiens 101-104 15662138-6 2005 Taken together, our data demonstrate that p33ING1b enhances taxol-induced apoptosis through p53-dependent pathway in human osteosarcoma cells. Paclitaxel 60-65 tumor protein p53 Homo sapiens 92-95 15467449-6 2004 Together, these findings suggest that p21(Cip1/WAF1) partially protects p53-null human leukemia cells from paclitaxel-mediated lethality, and raise the possibility that p21(Cip1/WAF1)-associated perturbations in signal transduction pathways as well as Bcl-2 phosphorylation status may play a role in this phenomenon. Paclitaxel 107-117 tumor protein p53 Homo sapiens 72-75 16127286-8 2005 Although untreated mutant p53 tumors may be responsive to first-line paclitaxel-containing therapy, it is likely that loss of p53 leads to genomic instability resulting in rapid progression to drug resistance. Paclitaxel 69-79 tumor protein p53 Homo sapiens 26-29 15031599-12 2004 CONCLUSIONS: p53-independent mitochondrial pathways and stress-reaction-induced pathways play critical roles in PTX-induced apoptosis in ovarian cancer cells. Paclitaxel 112-115 tumor protein p53 Homo sapiens 13-16 15159015-4 2004 Furthermore, combined administrations of insulin and paclitaxel affected MAPK pathway, Raf-1 activation and p53 expression levels. Paclitaxel 53-63 tumor protein p53 Homo sapiens 108-111 15012603-5 2004 Evidence is presented that the effects of taxol on ER alpha gene transcription may be mediated through the induction of p53. Paclitaxel 42-47 tumor protein p53 Homo sapiens 120-123 15475475-6 2004 Paclitaxel activated p53 protein at low concentrations but exhibited G2/M cell cycle blocking activity at higher concentrations where microtubules were stabilized. Paclitaxel 0-10 tumor protein p53 Homo sapiens 21-24 15486197-7 2004 In addition, paclitaxel, at cytostatic concentrations, early initiates an apoptotic signaling pathway associated with increases in the mitochondrial reducing potential, mitochondrial membrane potential, p53 expression, and Bax/Bcl-2 ratio. Paclitaxel 13-23 tumor protein p53 Homo sapiens 203-206 12802925-9 2003 Moreover, TMBL-1 cells are sensitive to paclitaxel, which could induce p53-independent apoptosis. Paclitaxel 40-50 tumor protein p53 Homo sapiens 71-74 12771935-3 2003 Following 8 h of exposure to taxol, the cell line DoHH2 (p53 wild type) exhibited mitotic arrest and engagement of apoptosis, whereas the cell line SU-DHL-4 (p53 mutant) breached cell-cycle arrest with progression to an abnormal cycle and a 24 h delay in the engagement of apoptosis. Paclitaxel 29-34 tumor protein p53 Homo sapiens 57-60 12771935-3 2003 Following 8 h of exposure to taxol, the cell line DoHH2 (p53 wild type) exhibited mitotic arrest and engagement of apoptosis, whereas the cell line SU-DHL-4 (p53 mutant) breached cell-cycle arrest with progression to an abnormal cycle and a 24 h delay in the engagement of apoptosis. Paclitaxel 29-34 tumor protein p53 Homo sapiens 158-161 12684687-4 2003 We report that Brca1-deficiency in p53-null cells was associated with increased sensitivity to the topoisomerase I poisons camptothecin and topotecan, the topoisomerase II poisons doxorubicin, mitoxantrone and etoposide, and to the platinum compounds carboplatin and oxaliplatin, but not to the antimetabolites 5-fluorouracil and gemcitabine and the taxanes docetaxel and paclitaxel. Paclitaxel 372-382 tumor protein p53 Homo sapiens 35-38 12715164-0 2003 p53 expression and resistance against paclitaxel in patients with metastatic breast cancer. Paclitaxel 38-48 tumor protein p53 Homo sapiens 0-3 12715164-13 2003 CONCLUSION: The immunohistochemical detection of p53 characterizes patients with metastatic breast cancer unlikely to respond to paclitaxel. Paclitaxel 129-139 tumor protein p53 Homo sapiens 49-52 14751837-6 2003 The antisense oligonucleotides also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel. Paclitaxel 179-189 tumor protein p53 Homo sapiens 63-66 12860987-1 2003 Modification-specific antibodies were used to characterize the phosphorylation and acetylation of human p53 in response to genotoxic (UV, IR, and adriamycin) and non-genotoxic (PALA, taxol, nocodazole) stress in cultured human cells at 14 known modification sites. Paclitaxel 183-188 tumor protein p53 Homo sapiens 104-107 12860987-5 2003 The non-genotoxic agents PALA, taxol and nocodazole induced p53 accumulation and phosphorylation at Ser6, Ser33, Ser46, and Ser392. Paclitaxel 31-36 tumor protein p53 Homo sapiens 60-63 12897130-0 2003 Silencing of the novel p53 target gene Snk/Plk2 leads to mitotic catastrophe in paclitaxel (taxol)-exposed cells. Paclitaxel 80-90 tumor protein p53 Homo sapiens 23-26 12897130-0 2003 Silencing of the novel p53 target gene Snk/Plk2 leads to mitotic catastrophe in paclitaxel (taxol)-exposed cells. Paclitaxel 92-97 tumor protein p53 Homo sapiens 23-26 12897130-6 2003 Since siRNA directed against Snk/Plk2 promoted death of paclitaxel-treated cells in mitosis, we envision a mitotic checkpoint wherein p53-dependent activation of Snk/Plk2 prevents mitotic catastrophe following spindle damage. Paclitaxel 56-66 tumor protein p53 Homo sapiens 134-137 12761496-3 2003 We demonstrated here that low doses of PTX that are unable to activate the spindle assembly checkpoint, upregulate p21 by a p53-dependent pathway and induce its translocation to the cytoplasm. Paclitaxel 39-42 tumor protein p53 Homo sapiens 124-127 26680929-2 2003 In this study, to further demonstrate the differential effect of the tumor suppressor gene, p53, on the Taxol-induced apoptosis in osteogenic sarcoma cell lines, we used p53-defected SaOS2 cells and wild type p53-expressed U2OS cells. Paclitaxel 104-109 tumor protein p53 Homo sapiens 92-95 26680929-4 2003 To examine whether the differential expressions of p53, in U2OS and SaOS2 cells, were associated with Taxol-induced apoptosis, DNA fragmentation assays were performed on both cytosolic and genomic DNA. Paclitaxel 102-107 tumor protein p53 Homo sapiens 51-54 26680929-12 2003 CONCLUSION: From these results, it was concluded that p53-defected SaOS2 cells are much more sensitive to Taxol-induced apoptosis than p53-expressed U2OS cells. Paclitaxel 106-111 tumor protein p53 Homo sapiens 54-57 26680929-6 2003 RESULTS: The cell viability of the p53-defected SaOS2 cells was markedly decreased with Taxol treatment. Paclitaxel 88-93 tumor protein p53 Homo sapiens 35-38 12684432-0 2003 Low-dose fractionated radiation potentiates the effects of Paclitaxel in wild-type and mutant p53 head and neck tumor cell lines. Paclitaxel 59-69 tumor protein p53 Homo sapiens 94-97 12684432-7 2003 The cell cycle regulator p53 and its target genes p21(waf1/cip1) and BAX were induced in SCC-61 cells treated with 2 Gy, Paclitaxel, or in combination, but not in SQ-20B cells. Paclitaxel 121-131 tumor protein p53 Homo sapiens 25-28 26680929-10 2003 The Taxol-induced apoptosis in p53 defected-osteogenic sarcoma cells was associated with the PARP cleavage as a result of the increased activity of caspase 3, and the high expressions of cyclin B1 and PLK. Paclitaxel 4-9 tumor protein p53 Homo sapiens 31-34 12618886-2 2003 Amifostine induced a G1 arrest and protected against paclitaxel toxicity in p53-proficient but not in p53-deficient cells. Paclitaxel 53-63 tumor protein p53 Homo sapiens 76-79 12518324-7 2003 The antisense oligonucleotide also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel. Paclitaxel 178-188 tumor protein p53 Homo sapiens 62-65 12598349-0 2003 Correlation of p53 status with outcome of neoadjuvant chemotherapy using paclitaxel and doxorubicin in stage IIIB breast cancer. Paclitaxel 73-83 tumor protein p53 Homo sapiens 15-18 12530065-0 2002 Reduced expression of p53 and p21WAF1/CIP1 sensitizes human breast cancer cells to paclitaxel and its combination with 5-fluorouracil. Paclitaxel 83-93 tumor protein p53 Homo sapiens 22-25 12530065-6 2002 RESULTS: Tumor cells transfected with antisense p53 or p21WAF1/CIP1 exhibited a significant increase in their sensitivity to paclitaxel. Paclitaxel 125-135 tumor protein p53 Homo sapiens 48-51 12530065-7 2002 The reduced protein levels of p53 and p21WAF1/CIP1 were also found to abrogate the inhibitory effects of 5-FU on paclitaxel-induced mitotic arrest and apoptosis. Paclitaxel 113-123 tumor protein p53 Homo sapiens 30-33 12530065-8 2002 CONCLUSION: These findings suggest that the status of p53 and p21WAF1/CIP1 might play an important role in tumor cell susceptibility to paclitaxel and its combination with other drugs such as 5-FU. Paclitaxel 136-146 tumor protein p53 Homo sapiens 54-57 12142057-4 2002 Notably, the simultaneous exposure to ZD0473 and paclitaxel for 96 h resulted in synergy (as defined by a median effect analysis) in all four cell lines (i.e. independent of cisplatin resistance and p53 status). Paclitaxel 49-59 tumor protein p53 Homo sapiens 199-202 12175696-1 2002 The correlation between inactivation of the TP53 gene through mutation or the presence of high-risk human papillomavirus (HPV) DNA and intrinsic paclitaxel sensitivity was studied in 27 gynaecological cancer cell lines. Paclitaxel 145-155 tumor protein p53 Homo sapiens 44-48 12214265-1 2002 By inducing p53-dependent G2 arrest, the pretreatment with low concentrations of DNA damaging drugs (e.g., doxorubicin, DOX) can prevent cell death caused by microtubule-active drugs (e.g., paclitaxel, PTX), thus potentially permitting selective killing of p53-deficient cancer cells. Paclitaxel 190-200 tumor protein p53 Homo sapiens 12-15 11244509-6 2001 p53 phosphorylation also varied in a MTI-dependent manner, as Taxol and Vincristine induced more p53 phospho-forms than nocodazole. Paclitaxel 62-67 tumor protein p53 Homo sapiens 0-3 12432259-2 2002 By causing p53-mediated arrest, pretreatment with low concentrations of doxorubicin (DOX) protected HCT116 cells from the cytotoxicity caused by PTX. Paclitaxel 145-148 tumor protein p53 Homo sapiens 11-14 12440809-7 2002 Conversely, experimental and clinical data seem to show that paclitaxel enhances apoptosis through a p53-independent pathway, that probably involves the Bax gene. Paclitaxel 61-71 tumor protein p53 Homo sapiens 101-104 12440809-8 2002 Whereas patients with wild-type p53 tumors have a good chance to respond to platinum, patients with mutant p53 tumors may have a clinical benefit from the addition of paclitaxel to platinum-based chemotherapy. Paclitaxel 167-177 tumor protein p53 Homo sapiens 107-110 11728383-6 2001 We also observed that a paclitaxel-resistant cell line expressed Bax at a much lower level than the sensitive parental line [A2780(1A9)], consistent with its mutant p53 status. Paclitaxel 24-34 tumor protein p53 Homo sapiens 165-168 11458051-0 2001 Functional p53 mutation as a molecular determinant of paclitaxel and gemcitabine susceptibility in human bladder cancer. Paclitaxel 54-64 tumor protein p53 Homo sapiens 11-14 11458051-4 2001 Susceptibility of these inducible p53 TCC cells to paclitaxel and gemcitabine induced cytotoxicity was evaluated and kill significance determined between sub-lethal and lethal doses. Paclitaxel 51-61 tumor protein p53 Homo sapiens 34-37 11458051-5 2001 RESULTS: Significant paclitaxel dose dependent cytotoxicity was observed in J82 TCC cells lacking normal p53 and tsp53 transfected cells at 37C, which was the mutant p53 temperature in transfectants between maximal and minimal kill concentrations for either (p <0.001). Paclitaxel 21-31 tumor protein p53 Homo sapiens 105-108 11458051-5 2001 RESULTS: Significant paclitaxel dose dependent cytotoxicity was observed in J82 TCC cells lacking normal p53 and tsp53 transfected cells at 37C, which was the mutant p53 temperature in transfectants between maximal and minimal kill concentrations for either (p <0.001). Paclitaxel 21-31 tumor protein p53 Homo sapiens 115-118 11458051-8 2001 CONCLUSIONS: Paclitaxel requires functionally mutated p53 to induce cell death in human bladder cells, indicating that it may be more effective against TCC with p53 mutations than against TCC, which lacks p53 abnormalities, while gemcitabine is effective regardless of p53 function. Paclitaxel 13-23 tumor protein p53 Homo sapiens 54-57 11458051-8 2001 CONCLUSIONS: Paclitaxel requires functionally mutated p53 to induce cell death in human bladder cells, indicating that it may be more effective against TCC with p53 mutations than against TCC, which lacks p53 abnormalities, while gemcitabine is effective regardless of p53 function. Paclitaxel 13-23 tumor protein p53 Homo sapiens 161-164 11458051-8 2001 CONCLUSIONS: Paclitaxel requires functionally mutated p53 to induce cell death in human bladder cells, indicating that it may be more effective against TCC with p53 mutations than against TCC, which lacks p53 abnormalities, while gemcitabine is effective regardless of p53 function. Paclitaxel 13-23 tumor protein p53 Homo sapiens 161-164 11458051-8 2001 CONCLUSIONS: Paclitaxel requires functionally mutated p53 to induce cell death in human bladder cells, indicating that it may be more effective against TCC with p53 mutations than against TCC, which lacks p53 abnormalities, while gemcitabine is effective regardless of p53 function. Paclitaxel 13-23 tumor protein p53 Homo sapiens 161-164 11439344-0 2001 Low concentrations of paclitaxel induce cell type-dependent p53, p21 and G1/G2 arrest instead of mitotic arrest: molecular determinants of paclitaxel-induced cytotoxicity. Paclitaxel 22-32 tumor protein p53 Homo sapiens 60-63 11439344-3 2001 At these low concentrations that are insufficient to inhibit mitotic progression, PTX induced both p53 and p21 causing G1 and G2 arrest in A549. Paclitaxel 82-85 tumor protein p53 Homo sapiens 99-102 11484935-2 2001 We found that four anticancer agents: etoposide, doxorubicin, bleomycin and paclitaxel induced apoptosis in human umbilical vein endothelial cells (HUVECs) (as judged by DNA fragmentation) with a time- and concentration-dependent decrease in bcl-2 protein but without the involvement of p53. Paclitaxel 76-86 tumor protein p53 Homo sapiens 287-290 11356930-5 2001 In nontransformed cells, WR-1065 protected cells from the cytotoxic effects of paclitaxel in a p53-dependent manner. Paclitaxel 79-89 tumor protein p53 Homo sapiens 95-98 11295099-0 2001 Regulation of BRCA1 and BRCA2 transcript in response to cisplatin, adriamycin, taxol and ionising radiation is correlated to p53 functional status in ovarian cancer cell lines. Paclitaxel 79-84 tumor protein p53 Homo sapiens 125-128 12150453-3 2002 Taxol treatment resulted in elevated expression of p53 and of p21, which was more pronounced and persistent in cyclin D1 overexpressing cells. Paclitaxel 0-5 tumor protein p53 Homo sapiens 51-54 12168940-0 2002 Correlation of clinical outcome with p53 and p21 status in patients with advanced transitional-cell carcinoma treated with paclitaxel and carboplatin. Paclitaxel 123-133 tumor protein p53 Homo sapiens 37-40 12168940-1 2002 BACKGROUND: The purpose of the present study was to correlate the nuclear expression of p53 and p21 with response to paclitaxel and carboplatin, progression-free survival (PFS) as well as overall survival (OS), in patients with urothelial metastatic transitional-cell carcinoma (TCC). Paclitaxel 117-127 tumor protein p53 Homo sapiens 88-91 11774260-0 2002 Apoptosis induced by low-dose paclitaxel is associated with p53 upregulation in nasopharyngeal carcinoma cells. Paclitaxel 30-40 tumor protein p53 Homo sapiens 60-63 11774260-6 2002 We showed that paclitaxel inhibited growth and induced apoptosis in both cell lines but that the p53 mutant line (CNE-2) was less sensitive to treatment with low-dose paclitaxel. Paclitaxel 167-177 tumor protein p53 Homo sapiens 97-100 11774260-8 2002 We observed a striking increase of p53 protein levels in NPC cells exposed to 1 and 10 nM paclitaxel but a marked inhibition at 100 nM paclitaxel treatment. Paclitaxel 90-100 tumor protein p53 Homo sapiens 35-38 11774260-8 2002 We observed a striking increase of p53 protein levels in NPC cells exposed to 1 and 10 nM paclitaxel but a marked inhibition at 100 nM paclitaxel treatment. Paclitaxel 135-145 tumor protein p53 Homo sapiens 35-38 11774260-10 2002 In summary, low-dose paclitaxel inhibited cell growth in NPC cells and induced apoptosis possibly by upregulation of p53. Paclitaxel 21-31 tumor protein p53 Homo sapiens 117-120 11505395-2 2001 This combination also enhanced sensitivity to paclitaxel in a bcl-2 and mutant p53 expressing renal carcinoma cell line. Paclitaxel 46-56 tumor protein p53 Homo sapiens 79-82 11439344-5 2001 Furthermore, we observed that the levels of p53 and p21 induced by adriamycin and by low concentrations of PTX in A549 cells were comparable. Paclitaxel 107-110 tumor protein p53 Homo sapiens 44-47 11439344-6 2001 This observation led us to conclude that low concentrations of PTX can induce p53 and p21 sufficiently to cause G1 and G2. Paclitaxel 63-66 tumor protein p53 Homo sapiens 78-81 11275363-0 2001 Taxol-induced cell cycle arrest and apoptosis: dose-response relationship in lung cancer cells of different wild-type p53 status and under isogenic condition. Paclitaxel 0-5 tumor protein p53 Homo sapiens 118-121 11275363-3 2001 DNA content analyses in A 549 (p53, +/+) and H 1299 (p53, -/-) cells, showed that taxol progressively induced G2/M arrest in both cell lines in a concentration-dependent manner, which was accompanied by a parallel decrease in the G1 population. Paclitaxel 82-87 tumor protein p53 Homo sapiens 31-34 11275363-3 2001 DNA content analyses in A 549 (p53, +/+) and H 1299 (p53, -/-) cells, showed that taxol progressively induced G2/M arrest in both cell lines in a concentration-dependent manner, which was accompanied by a parallel decrease in the G1 population. Paclitaxel 82-87 tumor protein p53 Homo sapiens 53-56 11313944-0 2001 Taxol-induced apoptosis depends on MAP kinase pathways (ERK and p38) and is independent of p53. Paclitaxel 0-5 tumor protein p53 Homo sapiens 91-94 11313944-4 2001 We found that Taxol treatment strongly activated ERK, p38 MAP kinase and p53 in MAP kinase MCF7 cells prior to apoptosis. Paclitaxel 14-19 tumor protein p53 Homo sapiens 73-76 11313944-8 2001 However, cells with inactivated p53, unlike cells harboring wild type p53, failed to arrest in G2/M after treatment with Taxol and continued to divide or go into apoptosis. Paclitaxel 121-126 tumor protein p53 Homo sapiens 32-35 11313944-9 2001 Our data show that both ERK and p38 MAP kinase cascades are essential for apoptotic response to Taxol-induced cellular killing and are independent of p53 activity. Paclitaxel 96-101 tumor protein p53 Homo sapiens 150-153 11313944-10 2001 However, p53 may serve as a survival factor in breast carcinoma cells treated with Taxol by blocking cells in G2/M phase of the cell cycle. Paclitaxel 83-88 tumor protein p53 Homo sapiens 9-12 11244509-9 2001 Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53. Paclitaxel 67-72 tumor protein p53 Homo sapiens 127-130 11244509-9 2001 Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53. Paclitaxel 67-72 tumor protein p53 Homo sapiens 127-130 11244509-9 2001 Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53. Paclitaxel 212-217 tumor protein p53 Homo sapiens 127-130 11244509-9 2001 Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53. Paclitaxel 212-217 tumor protein p53 Homo sapiens 127-130 11326311-0 2001 Cisplatinum and taxol induce different patterns of p53 phosphorylation. Paclitaxel 16-21 tumor protein p53 Homo sapiens 51-54 11326311-1 2001 Posttranslational modifications of p53 induced by two widely used anticancer agents, cisplatinum (DDP) and taxol were investigated in two human cancer cell lines. Paclitaxel 107-112 tumor protein p53 Homo sapiens 35-38 11205220-1 2000 BACKGROUND: The aim of this study was to assess the relationship between p53 status and the clinical outcome of patients with advanced ovarian cancer treated with a paclitaxel-based regimen. Paclitaxel 165-175 tumor protein p53 Homo sapiens 73-76 11175336-11 2000 Additionally, the human prostate cancer cell line, LNCaP, also formed nuclear Bax/p53 complexes only after apoptosis was induced by paclitaxel. Paclitaxel 132-142 tumor protein p53 Homo sapiens 82-85 11099323-2 2000 Because taxanes could induce p53-independent apoptosis, we assessed the relevance of p53 gene status to response in ovarian carcinoma patients receiving paclitaxel and platinum-containing chemotherapy. Paclitaxel 153-163 tumor protein p53 Homo sapiens 85-88 11099323-14 2000 CONCLUSION: In contrast to the limited efficacy of treatment with paclitaxel in combination with standard platinum doses against wild-type p53 ovarian tumors, patients with mutant p53 ovarian tumors were more responsive to paclitaxel-based chemotherapy. Paclitaxel 66-76 tumor protein p53 Homo sapiens 139-142 11099323-14 2000 CONCLUSION: In contrast to the limited efficacy of treatment with paclitaxel in combination with standard platinum doses against wild-type p53 ovarian tumors, patients with mutant p53 ovarian tumors were more responsive to paclitaxel-based chemotherapy. Paclitaxel 223-233 tumor protein p53 Homo sapiens 180-183 11205220-9 2000 These results are consistent with experimental data showing that paclitaxel cytotoxicity in ovarian cancer is likely to be mediated by a p53-independent pathway. Paclitaxel 65-75 tumor protein p53 Homo sapiens 137-140 11064345-0 2000 Low dose fractionated radiation enhances the radiosensitization effect of paclitaxel in colorectal tumor cells with mutant p53. Paclitaxel 74-84 tumor protein p53 Homo sapiens 123-126 11064345-1 2000 BACKGROUND: The current study was undertaken to investigate the influence of wild-type or mutant p53 status on the radiosensitizing effect of paclitaxel in colorectal tumor cell lines. Paclitaxel 142-152 tumor protein p53 Homo sapiens 97-100 11034077-2 2000 A2780 human ovarian carcinoma cells, which are sensitive to cisplatin and paclitaxel, express wild-type p53 and exhibit a p53-mediated increase in p21 in response to the chemotherapeutic agents. Paclitaxel 74-84 tumor protein p53 Homo sapiens 122-125 11129289-4 2000 Paclitaxel was chosen for combination therapy in the preclinical study reported here due to its extensive use as a first-line therapy in ovarian cancer, its synergy with SCH58500 in preclinical cancer models, and its activation of p53-independent apoptosis, which might result in a "lowered threshold" for tumor cell death. Paclitaxel 0-10 tumor protein p53 Homo sapiens 231-234 11025661-2 2000 Treatment with vincristine or paclitaxel before DNA-damage or before leptomycin B treatment reduces nuclear accumulation of p53 and expression of mdm2 and p21. Paclitaxel 30-40 tumor protein p53 Homo sapiens 124-127 11899648-1 2000 This study assesses the potential value of the tumor markers p53, HER2, and Bcl-2 in predicting the clinical response to doxorubicin and paclitaxel as single agents in the treatment of metastatic breast cancer. Paclitaxel 137-147 tumor protein p53 Homo sapiens 61-64 11070791-4 2000 Restoration of p53 protein function in LN382 cells at 34 degrees C reduced the cytotoxicity of etoposide and paclitaxel, whereas that of cisplatin and ACNU was not affected. Paclitaxel 109-119 tumor protein p53 Homo sapiens 15-18 10974635-1 2000 We conducted this study to determine whether the sensitivity of ovarian cancer cells to paclitaxel (PTX) relates to cells undergoing p53-dependent apoptosis. Paclitaxel 88-98 tumor protein p53 Homo sapiens 133-136 10974635-1 2000 We conducted this study to determine whether the sensitivity of ovarian cancer cells to paclitaxel (PTX) relates to cells undergoing p53-dependent apoptosis. Paclitaxel 100-103 tumor protein p53 Homo sapiens 133-136 10974635-3 2000 In SK-OV-3 and KP cells, which have a homozygous deletion of the TP53 gene, wild-type TP53 gene-transduction markedly enhanced the sensitivity to cisplatin (CDDP), but did not enhance the sensitivity to PTX. Paclitaxel 203-206 tumor protein p53 Homo sapiens 65-69 10974635-3 2000 In SK-OV-3 and KP cells, which have a homozygous deletion of the TP53 gene, wild-type TP53 gene-transduction markedly enhanced the sensitivity to cisplatin (CDDP), but did not enhance the sensitivity to PTX. Paclitaxel 203-206 tumor protein p53 Homo sapiens 86-90 11070791-8 2000 These results indicate that cell cycle arrest induced by wild-type p53 function may abrogate the cytotoxic effects of etoposide and paclitaxel, which are dependent on G2M-associated apoptosis. Paclitaxel 132-142 tumor protein p53 Homo sapiens 67-70 10854551-0 2000 Raf-1 kinase activity predicts for paclitaxel resistance in TP53mut, but not TP53wt human ovarian cancer cells. Paclitaxel 35-45 tumor protein p53 Homo sapiens 60-67 10993958-5 2000 Additional cell loss occurred in 40-16 and HCT116 p53-/- cells following administration of Taxol before IR and 5-FU. Paclitaxel 91-96 tumor protein p53 Homo sapiens 50-53 10951339-9 2000 The 1-year survival rates for patients with and without p53 mutation after treatment with weekly paclitaxel were 63% (95% confidence interval [CI], 31-100%) and 53% (95% CI, 33-86%), respectively. Paclitaxel 97-107 tumor protein p53 Homo sapiens 56-59 10951339-11 2000 These results provide clinical support for in vitro observations that paclitaxel can bypass mutant p53 and lead to tumor cell death by alternate pathway(s). Paclitaxel 70-80 tumor protein p53 Homo sapiens 99-102 10951339-12 2000 Paclitaxel should be considered as a component of treatment for patients with metastatic NSCLC with tumors that have p53 mutations. Paclitaxel 0-10 tumor protein p53 Homo sapiens 117-120 10854551-0 2000 Raf-1 kinase activity predicts for paclitaxel resistance in TP53mut, but not TP53wt human ovarian cancer cells. Paclitaxel 35-45 tumor protein p53 Homo sapiens 60-64 10854551-7 2000 However, in the ovarian cancer cell lines (CA-OV3, SK-OV3, 2780/CP and OAW42/CP) that have a mutant TP53 (TP53mut), the cytotoxicity induced by 60 nM paclitaxel exhibited the same relationship to Raf-1 kinase activity as previously observed in cervical tumor cell lines. Paclitaxel 150-160 tumor protein p53 Homo sapiens 100-104 10854551-7 2000 However, in the ovarian cancer cell lines (CA-OV3, SK-OV3, 2780/CP and OAW42/CP) that have a mutant TP53 (TP53mut), the cytotoxicity induced by 60 nM paclitaxel exhibited the same relationship to Raf-1 kinase activity as previously observed in cervical tumor cell lines. Paclitaxel 150-160 tumor protein p53 Homo sapiens 106-113 10854551-8 2000 These data suggest that the therapeutic efficacy of paclitaxel in ovarian cancer patient whose tumors have TP53mut might be increased if it is administered in combination with Raf-1 kinase inhibitors, e.g., ISIS 5132. Paclitaxel 52-62 tumor protein p53 Homo sapiens 107-111 10736495-13 2000 The high response rate to this regimen despite frequent p53 mutation is consistent with the p53-independent mechanism of paclitaxel. Paclitaxel 121-131 tumor protein p53 Homo sapiens 92-95 10871860-0 2000 Paclitaxel selects for mutant or pseudo-null p53 in drug resistance associated with tubulin mutations in human cancer. Paclitaxel 0-10 tumor protein p53 Homo sapiens 45-48 10871860-2 2000 While the role of p53 in the intrinsic sensitivity of human cancer cells to paclitaxel (PTX) remains controversial, its role in acquired paclitaxel resistance has never been addressed. Paclitaxel 76-86 tumor protein p53 Homo sapiens 18-21 10871860-3 2000 In this study we examined the p53 status of three paclitaxel selected human ovarian carcinoma sublines, resistant to paclitaxel due to acquired beta-tubulin mutations which impair paclitaxel"s interaction with tubulin. Paclitaxel 50-60 tumor protein p53 Homo sapiens 30-33 10871860-4 2000 In contrast to parental cells which have wt p53, in all PTX-resistant sublines p53 was functionally inactive. Paclitaxel 56-59 tumor protein p53 Homo sapiens 44-47 10871860-4 2000 In contrast to parental cells which have wt p53, in all PTX-resistant sublines p53 was functionally inactive. Paclitaxel 56-59 tumor protein p53 Homo sapiens 79-82 10871860-8 2000 While PTX resistance is primarily conferred by the tubulin mutations, the loss of functional p53 observed in all clones, suggests that this loss may facilitate the development of resistance potentially by providing a clonal advantage which promotes the isolation of paclitaxel resistant cells. Paclitaxel 266-276 tumor protein p53 Homo sapiens 93-96 10935506-0 2000 Driving p53 response to Bax activation greatly enhances sensitivity to taxol by inducing massive apoptosis. Paclitaxel 71-76 tumor protein p53 Homo sapiens 8-11 10935506-4 2000 The clones expressing bax under the control of p53 obtained from the wild-type (wt) p53-expressing cell line A2780 were much more sensitive (500- to 1000-fold) to the anticancer agent taxol than the parent cell line, with a higher percentage of cells undergoing apoptosis after drug treatment that was clearly p53-dependent and bax-mediated. Paclitaxel 184-189 tumor protein p53 Homo sapiens 47-50 10935506-4 2000 The clones expressing bax under the control of p53 obtained from the wild-type (wt) p53-expressing cell line A2780 were much more sensitive (500- to 1000-fold) to the anticancer agent taxol than the parent cell line, with a higher percentage of cells undergoing apoptosis after drug treatment that was clearly p53-dependent and bax-mediated. Paclitaxel 184-189 tumor protein p53 Homo sapiens 84-87 10935506-4 2000 The clones expressing bax under the control of p53 obtained from the wild-type (wt) p53-expressing cell line A2780 were much more sensitive (500- to 1000-fold) to the anticancer agent taxol than the parent cell line, with a higher percentage of cells undergoing apoptosis after drug treatment that was clearly p53-dependent and bax-mediated. Paclitaxel 184-189 tumor protein p53 Homo sapiens 84-87 10935506-7 2000 In conclusion, driving the p53 response (after taxol treatment) by activating the bax gene rather than the p21 gene results in induction of massive apoptosis, in vitro and in vivo, and greatly enhances sensitivity to the drug. Paclitaxel 47-52 tumor protein p53 Homo sapiens 27-30 10811471-5 2000 In contrast, Ad-p53 showed additive effects with the antitubulin agents (paclitaxel and docetaxel) in all four of the cell lines tested. Paclitaxel 73-83 tumor protein p53 Homo sapiens 16-19 10717242-0 2000 The effect of p53-function on the sensitivity to paclitaxel with or without hyperthermia in human colorectal carcinoma cells. Paclitaxel 49-59 tumor protein p53 Homo sapiens 14-17 10717242-1 2000 The importance of p53-function for the sensitivity to paclitaxel with and without hyperthermia (HT) was studied in an isogenic cell line system. Paclitaxel 54-64 tumor protein p53 Homo sapiens 18-21 10717242-2 2000 The inactivation of p53 decreased sensitivity to paclitaxel (1.1-2.5-fold), which correlated with a lower induction of apoptosis. Paclitaxel 49-59 tumor protein p53 Homo sapiens 20-23 10717242-5 2000 In conclusion, cellular sensitivity to paclitaxel depends on p53-function by its ability to induce apoptosis. Paclitaxel 39-49 tumor protein p53 Homo sapiens 61-64 10810342-6 2000 The sensitivity of wt p53-transfected cells (H358/p53) to paclitaxel was approximately 3-fold lower than that of H358 cells. Paclitaxel 58-68 tumor protein p53 Homo sapiens 22-25 10810342-6 2000 The sensitivity of wt p53-transfected cells (H358/p53) to paclitaxel was approximately 3-fold lower than that of H358 cells. Paclitaxel 58-68 tumor protein p53 Homo sapiens 50-53 11052631-0 2000 Multiple factors other than p53 influence colon cancer sensitivity to paclitaxel. Paclitaxel 70-80 tumor protein p53 Homo sapiens 28-31 10706117-10 2000 In addition, standard chemotherapeutic agents (paclitaxol and cisplatin) showed a synergistic effect when combined with ONYX-015, and this effect was p53 mutant dependent. Paclitaxel 47-57 tumor protein p53 Homo sapiens 150-153 10741907-10 2000 Meanwhile, Ad-p53 gene transfer combined with taxol, cisplatin, doxorubicin or mitomycin C was shown to be even more effective in suppressing growth in the two cell lines. Paclitaxel 46-51 tumor protein p53 Homo sapiens 14-17 10665656-10 1999 p53 gene transfection did not affect the extent of DNA fragmentation in either cell line, suggesting that paclitaxel may induce p53-independent apoptosis. Paclitaxel 106-116 tumor protein p53 Homo sapiens 128-131 10656431-9 2000 Combination of sequencing and IHC results revealed a significant association between abnormal p53 and response to paclitaxel (P = 0.011). Paclitaxel 114-124 tumor protein p53 Homo sapiens 94-97 10656431-11 2000 Whereas clinical response to FEC was found to be dependent on normal p53, the cytotoxicity of paclitaxel was related to defective p53. Paclitaxel 94-104 tumor protein p53 Homo sapiens 130-133 10656431-12 2000 The efficiency of paclitaxel during mitosis might be supported by lack of G1 arrest due to p53 deficiency. Paclitaxel 18-28 tumor protein p53 Homo sapiens 91-94 10656431-13 2000 Therefore, patients with p53-deficient tumors may benefit from paclitaxel. Paclitaxel 63-73 tumor protein p53 Homo sapiens 25-28 10534572-11 1999 Moreover, up-regulation of p53 and down-regulation of Bcl-2 was observed only in HPAC cells treated with Taxol. Paclitaxel 105-110 tumor protein p53 Homo sapiens 27-30 10697517-0 1999 Effect of paclitaxel pretreatment on radiation-induced p53-dependent apoptosis. Paclitaxel 10-20 tumor protein p53 Homo sapiens 55-58 10697517-1 1999 The aim of this study was to investigate the effect of paclitaxel on radiation-induced p53-dependent apoptosis. Paclitaxel 55-65 tumor protein p53 Homo sapiens 87-90 10697517-9 1999 The present study indicates that p53-dependent apoptosis was frequently induced in the human tumor in vivo by irradiation, but not by paclitaxel alone. Paclitaxel 134-144 tumor protein p53 Homo sapiens 33-36 10471519-1 1999 Recent studies on paclitaxel (Taxol), a microtubule-stabilizing agent and effective anti-cancer drug, have identified numerous cellular and molecular effects, such as induction of cytokines and tumor-suppressor genes, indirect cytotoxicity due to secretion of tumor necrosis factor, vast activation of signal-transduction pathways and selective activity against cells lacking functional p53. Paclitaxel 18-28 tumor protein p53 Homo sapiens 387-390 10471519-1 1999 Recent studies on paclitaxel (Taxol), a microtubule-stabilizing agent and effective anti-cancer drug, have identified numerous cellular and molecular effects, such as induction of cytokines and tumor-suppressor genes, indirect cytotoxicity due to secretion of tumor necrosis factor, vast activation of signal-transduction pathways and selective activity against cells lacking functional p53. Paclitaxel 30-35 tumor protein p53 Homo sapiens 387-390 10421546-0 1999 Paclitaxel sensitivity correlates with p53 status and DNA fragmentation, but not G2/M accumulation. Paclitaxel 0-10 tumor protein p53 Homo sapiens 39-42 10424768-7 1999 p53 and p21 protein content also increased markedly during paclitaxel exposure, accompanied by phosphorylation of Bcl-2. Paclitaxel 59-69 tumor protein p53 Homo sapiens 0-3 10554637-11 1999 Human lymphoblasts with mutated p53 (WTK1, LD50 = 75 microM) were more resistant to paclitaxel than wild type p53 cells (TK6, LD50 = 25 microM). Paclitaxel 84-94 tumor protein p53 Homo sapiens 32-35 10446979-6 1999 Increased expression of MAP4, which occurs when p53 is transcriptionally inactive, increases microtubule polymerization, paclitaxel binding, and sensitivity to paclitaxel, a drug that stabilizes polymerized microtubules. Paclitaxel 160-170 tumor protein p53 Homo sapiens 48-51 10421546-3 1999 Although initial studies demonstrated that various DNA-damaging agents can induce p53, more recent studies have also shown p53 induction following nonDNA-damaging agents, including paclitaxel. Paclitaxel 181-191 tumor protein p53 Homo sapiens 123-126 10421546-10 1999 RESULTS: A 4-fold increase in paclitaxel sensitivity was observed among RKO cells deficient in p53 function compared with wild-type RKO cells (IC 50: 4 nM, 1 nM, 1nM for RKO, RKO.p53.13, RC 10.3, respectively). Paclitaxel 30-40 tumor protein p53 Homo sapiens 95-98 10421546-10 1999 RESULTS: A 4-fold increase in paclitaxel sensitivity was observed among RKO cells deficient in p53 function compared with wild-type RKO cells (IC 50: 4 nM, 1 nM, 1nM for RKO, RKO.p53.13, RC 10.3, respectively). Paclitaxel 30-40 tumor protein p53 Homo sapiens 179-182 10421546-11 1999 The increased cytotoxic effect in RKO cells with inactive p53 correlated with an increased propensity towards micronucleation and DNA fragmentation following paclitaxel treatment. Paclitaxel 158-168 tumor protein p53 Homo sapiens 58-61 10421546-13 1999 CONCLUSIONS: RKO cells lacking functional p53 demonstrate significantly enhanced sensitivity to paclitaxel compared with that of wild-type RKO cells. Paclitaxel 96-106 tumor protein p53 Homo sapiens 42-45 10421546-15 1999 Although previous published reports of enhanced paclitaxel sensitivity in p53-deficient cells correlated this finding with increased G2/M arrest, we did not observe any significant correlation between paclitaxel-induced cell kill and the degree of mitotic arrest. Paclitaxel 48-58 tumor protein p53 Homo sapiens 74-77 10347252-7 1999 Overexpression of p21(waf1) in SaOs-2 cells lacking both p53 and functional retinoblastoma protein may decrease the G2-M arrest induced by paclitaxel due to suppression of the S-G2 checkpoint, resulting in a decreased apoptotic response of cells to paclitaxel. Paclitaxel 139-149 tumor protein p53 Homo sapiens 57-60 10210535-0 1999 Role of p53 and p16 gene alterations in determining response to concurrent paclitaxel and radiation in solid tumor. Paclitaxel 75-85 tumor protein p53 Homo sapiens 8-11 10210535-8 1999 Recent evidence suggests that paclitaxel is unique in its ability to activate apoptosis in tumor cells with p53 mutations in vitro and in vivo. Paclitaxel 30-40 tumor protein p53 Homo sapiens 108-111 10210540-5 1999 This finding suggested that paclitaxel/RT was a rational treatment approach for other malignancies that frequently harbor p53 mutations, such as upper gastrointestinal malignancies. Paclitaxel 28-38 tumor protein p53 Homo sapiens 122-125 9792903-5 1998 This suggested that paclitaxel/RT was a rationale treatment approach for other malignancies which frequently harbor p53 mutations such as upper gastrointestinal malignancies. Paclitaxel 20-30 tumor protein p53 Homo sapiens 116-119 10453723-5 1999 Ectopic expression of mutant and wild-type p53val135 attenuated taxol cytotoxicity in both T98G cells, which are mutant for p53, and LN-229 cells, which exhibit functional wild-type p53 activity. Paclitaxel 64-69 tumor protein p53 Homo sapiens 43-46 10453723-6 1999 Interestingly, wild-type p53val135 abrogated the taxol-imposed G2/M arrest in both cell lines. Paclitaxel 49-54 tumor protein p53 Homo sapiens 25-28 9865905-9 1998 The second finding that drug-induced apoptosis was equal or higher in tumors that expressed Pgp, p53, and Bcl-2 compared to tumors that did not express these proteins supports the use of paclitaxel in treating Pgp-, p53- and Bcl-2-positive tumors. Paclitaxel 187-197 tumor protein p53 Homo sapiens 97-100 9865905-9 1998 The second finding that drug-induced apoptosis was equal or higher in tumors that expressed Pgp, p53, and Bcl-2 compared to tumors that did not express these proteins supports the use of paclitaxel in treating Pgp-, p53- and Bcl-2-positive tumors. Paclitaxel 187-197 tumor protein p53 Homo sapiens 216-219 9865921-1 1998 Paclitaxel induces a cell cycle block at G2-M phase by preventing the depolymerization of microtubules and induces p53-independent apoptosis in many cancer cells. Paclitaxel 0-10 tumor protein p53 Homo sapiens 115-118 9772293-7 1998 The accumulated p53 was biochemically active, as measured in a transient transfection assay upon treatment with gemcitabine, cisplatin, etoposide, and Taxol. Paclitaxel 151-156 tumor protein p53 Homo sapiens 16-19 9772293-8 1998 Activity was dependent on the drug dose applied and proportional to the level of accumulated p53, except for Taxol-induced p53 accumulation which correlated inversely with p53 biochemical activity. Paclitaxel 109-114 tumor protein p53 Homo sapiens 123-126 9772293-8 1998 Activity was dependent on the drug dose applied and proportional to the level of accumulated p53, except for Taxol-induced p53 accumulation which correlated inversely with p53 biochemical activity. Paclitaxel 109-114 tumor protein p53 Homo sapiens 123-126 9633517-0 1998 Inactivation of p53 in a human ovarian cancer cell line increases the sensitivity to paclitaxel by inducing G2/M arrest and apoptosis. Paclitaxel 85-95 tumor protein p53 Homo sapiens 16-19 9703286-0 1998 Therapy effect of either paclitaxel or cyclophosphamide combination treatment in patients with epithelial ovarian cancer and relation to TP53 gene status. Paclitaxel 25-35 tumor protein p53 Homo sapiens 137-141 9703286-8 1998 When relapse-free survival was estimated for all patients with TP53 alterations in their tumours, a significant better outcome for the paclitaxel/cisplatin group was found compared with the patient group receiving cyclophosphamide and cisplatin therapy (P = 0.002). Paclitaxel 135-145 tumor protein p53 Homo sapiens 63-67 9633517-1 1998 Paclitaxel-induced cytotoxicity, cell cycle perturbation, and apoptosis were determined in a human ovarian cancer cell line expressing wt p53 (A2780) and in a subclone (A2780/E6) obtained upon transfection with the product of the E6 gene of the human papilloma virus HPV16. Paclitaxel 0-10 tumor protein p53 Homo sapiens 138-141 9633517-2 1998 The inactivation of wt p53 in A2780/E6 was verified by measuring the inability of the clone to induce p53 and p21 expression after paclitaxel treatment. Paclitaxel 131-141 tumor protein p53 Homo sapiens 23-26 9633517-3 1998 The p53-negative clone (A2780/E6) was approximately 50-fold more sensitive to paclitaxel than wt p53-expressing A2780 cells. Paclitaxel 78-88 tumor protein p53 Homo sapiens 4-7 9633517-5 1998 This different cell cycle arrest was accompanied by increased frequency of paclitaxel-induced p53-independent apoptosis. Paclitaxel 75-85 tumor protein p53 Homo sapiens 94-97 9472635-6 1998 Similarly, high concentrations of taxol were required to induce p53 activity in the p53 wild-type cell line LN-229. Paclitaxel 34-39 tumor protein p53 Homo sapiens 64-67 9584207-8 1998 These data suggest that apoptosis in A2780 and A2780/cp70 is associated with an increased level of Bak and 21 kDa Bax after drug-induced damage and that functional p53 may be required for this effect after cisplatin but not after paclitaxel. Paclitaxel 230-240 tumor protein p53 Homo sapiens 164-167 9661042-0 1998 Evidence of p53-induced apoptosis in cancer cells exposed to taxol. Paclitaxel 61-66 tumor protein p53 Homo sapiens 12-15 9584207-0 1998 Cisplatin- and paclitaxel-induced apoptosis of ovarian carcinoma cells and the relationship between bax and bak up-regulation and the functional status of p53. Paclitaxel 15-25 tumor protein p53 Homo sapiens 155-158 9584207-1 1998 We investigated the roles of p53 and Bcl-2 homologues in the induction of apoptosis by cisplatin and paclitaxel in wild-type p53-expressing human ovarian carcinoma cells and cisplatin-resistant derivatives that have lost p53 function. Paclitaxel 101-111 tumor protein p53 Homo sapiens 125-128 9584207-1 1998 We investigated the roles of p53 and Bcl-2 homologues in the induction of apoptosis by cisplatin and paclitaxel in wild-type p53-expressing human ovarian carcinoma cells and cisplatin-resistant derivatives that have lost p53 function. Paclitaxel 101-111 tumor protein p53 Homo sapiens 125-128 9636834-18 1998 Finally, the finding that Taxol was very effective in inducing apoptosis in resistant sublines with p53 mutation supports the expression of an intact p53-independent pathway of apoptosis and suggests the pharmacological interest of Taxol in the treatment of p53-mutated tumors. Paclitaxel 26-31 tumor protein p53 Homo sapiens 100-103 9636834-18 1998 Finally, the finding that Taxol was very effective in inducing apoptosis in resistant sublines with p53 mutation supports the expression of an intact p53-independent pathway of apoptosis and suggests the pharmacological interest of Taxol in the treatment of p53-mutated tumors. Paclitaxel 26-31 tumor protein p53 Homo sapiens 150-153 9636834-18 1998 Finally, the finding that Taxol was very effective in inducing apoptosis in resistant sublines with p53 mutation supports the expression of an intact p53-independent pathway of apoptosis and suggests the pharmacological interest of Taxol in the treatment of p53-mutated tumors. Paclitaxel 26-31 tumor protein p53 Homo sapiens 150-153 9636834-18 1998 Finally, the finding that Taxol was very effective in inducing apoptosis in resistant sublines with p53 mutation supports the expression of an intact p53-independent pathway of apoptosis and suggests the pharmacological interest of Taxol in the treatment of p53-mutated tumors. Paclitaxel 232-237 tumor protein p53 Homo sapiens 100-103 9636834-18 1998 Finally, the finding that Taxol was very effective in inducing apoptosis in resistant sublines with p53 mutation supports the expression of an intact p53-independent pathway of apoptosis and suggests the pharmacological interest of Taxol in the treatment of p53-mutated tumors. Paclitaxel 232-237 tumor protein p53 Homo sapiens 150-153 9636834-18 1998 Finally, the finding that Taxol was very effective in inducing apoptosis in resistant sublines with p53 mutation supports the expression of an intact p53-independent pathway of apoptosis and suggests the pharmacological interest of Taxol in the treatment of p53-mutated tumors. Paclitaxel 232-237 tumor protein p53 Homo sapiens 150-153 9563876-15 1998 In the p53null SK-OV-3 xenograft model of ovarian cancer, a dosing schedule of p53 Ad that, by itself, had a relatively minimal effect on tumor burden (16%) caused a much greater decrease in tumor burden (55%) when combined with paclitaxel. Paclitaxel 229-239 tumor protein p53 Homo sapiens 7-10 9563876-15 1998 In the p53null SK-OV-3 xenograft model of ovarian cancer, a dosing schedule of p53 Ad that, by itself, had a relatively minimal effect on tumor burden (16%) caused a much greater decrease in tumor burden (55%) when combined with paclitaxel. Paclitaxel 229-239 tumor protein p53 Homo sapiens 79-82 9563876-17 1998 In summary, p53 Ad for cancer shows enhanced efficacy when combined with paclitaxel. Paclitaxel 73-83 tumor protein p53 Homo sapiens 12-15 9563901-1 1998 In the present study, we report our findings on the impact of p53 disruption on the sensitivity of human cell lines to the antimitotic agents Taxol and vincristine. Paclitaxel 142-147 tumor protein p53 Homo sapiens 62-65 9563901-5 1998 We also found that contrary to gamma-irradiation, Taxol and vincristine could induce apoptosis in lymphoma cell lines harboring p53 mutations. Paclitaxel 50-55 tumor protein p53 Homo sapiens 128-131 9563901-9 1998 The effect of p53 disruption on Taxol sensitivity was explored further in the breast carcinoma MCF-7 and colon carcinoma HCT-116 cell lines that had been stably transfected with either the human papillomavirus type-16 E6 gene or a dominant-negative mutant p53 gene. Paclitaxel 32-37 tumor protein p53 Homo sapiens 14-17 9472635-6 1998 Similarly, high concentrations of taxol were required to induce p53 activity in the p53 wild-type cell line LN-229. Paclitaxel 34-39 tumor protein p53 Homo sapiens 84-87 8943066-0 1996 BAX enhances paclitaxel-induced apoptosis through a p53-independent pathway. Paclitaxel 13-23 tumor protein p53 Homo sapiens 52-55 9815592-6 1997 The SKOV3ip1 cells do not express p53 protein; hence, the induction of apoptosis by paclitaxel is through a p53-independent pathway. Paclitaxel 84-94 tumor protein p53 Homo sapiens 108-111 9206986-9 1997 This suggested that paclitaxel/RT would be a rational treatment approach for other malignancies with a high frequency of p53 mutations, such as gastric and pancreatic cancers. Paclitaxel 20-30 tumor protein p53 Homo sapiens 121-124 9108094-3 1997 Taxol (paclitaxel) is more effective in the presence of mutant p53. Paclitaxel 0-5 tumor protein p53 Homo sapiens 63-66 9108094-3 1997 Taxol (paclitaxel) is more effective in the presence of mutant p53. Paclitaxel 7-17 tumor protein p53 Homo sapiens 63-66 9108094-13 1997 The synergistic therapeutic effect of Taxol with (90)Y-ChL6 may relate to the p53 mutant status and BCL2 expression in HBT 3477 cells, observations that increase the likelihood that the results of this study are relevant to therapy for breast cancer in patients. Paclitaxel 38-43 tumor protein p53 Homo sapiens 78-81 9041188-4 1997 By using for each cell line the paclitaxel IC50, we found that these concentrations were sufficient to induce an increase in p53 levels in all of the four wt p53-expressing cells, whereas in the mutated p53-expressing cells, the levels were unaffected. Paclitaxel 32-42 tumor protein p53 Homo sapiens 125-128 9041188-4 1997 By using for each cell line the paclitaxel IC50, we found that these concentrations were sufficient to induce an increase in p53 levels in all of the four wt p53-expressing cells, whereas in the mutated p53-expressing cells, the levels were unaffected. Paclitaxel 32-42 tumor protein p53 Homo sapiens 158-161 9041188-4 1997 By using for each cell line the paclitaxel IC50, we found that these concentrations were sufficient to induce an increase in p53 levels in all of the four wt p53-expressing cells, whereas in the mutated p53-expressing cells, the levels were unaffected. Paclitaxel 32-42 tumor protein p53 Homo sapiens 158-161 8521385-0 1995 Microtubule-active drugs taxol, vinblastine, and nocodazole increase the levels of transcriptionally active p53. Paclitaxel 25-30 tumor protein p53 Homo sapiens 108-111 8564846-0 1996 Loss of normal p53 function confers sensitization to Taxol by increasing G2/M arrest and apoptosis. Paclitaxel 53-58 tumor protein p53 Homo sapiens 15-18 8564846-2 1996 Normal human fibroblasts depleted of functional p53 by SV40 T antigen or HPV-16 E6, and primary embryo fibroblasts from p53 null mice showed seven- to ninefold increased cytotoxicity by paclitaxel. Paclitaxel 186-196 tumor protein p53 Homo sapiens 120-123 8564846-3 1996 Reduced levels of p53 correlated with increased G2/M phase arrest, micronucleation, and p53-independent paclitaxel-induced apoptosis. Paclitaxel 104-114 tumor protein p53 Homo sapiens 18-21 8564846-3 1996 Reduced levels of p53 correlated with increased G2/M phase arrest, micronucleation, and p53-independent paclitaxel-induced apoptosis. Paclitaxel 104-114 tumor protein p53 Homo sapiens 88-91 8826941-3 1996 In vitro data and animal studies suggest that paclitaxel may have a unique ability to activate tumor cell apoptosis in the absence of wild-type p53 function. Paclitaxel 46-56 tumor protein p53 Homo sapiens 144-147 8826941-4 1996 The authors sought to determine whether p53 mutations affect response to paclitaxel/RT in patients with locally advanced NSCLC. Paclitaxel 73-83 tumor protein p53 Homo sapiens 40-43 8826941-13 1996 These results suggest that paclitaxel/RT may be an active regimen for patients with other locally advanced neoplasms with high rates of p53 gene mutations. Paclitaxel 27-37 tumor protein p53 Homo sapiens 136-139 8763853-0 1996 The interaction of taxol and vinblastine with radiation induction of p53 and p21 WAF1/CIP1. Paclitaxel 19-24 tumor protein p53 Homo sapiens 69-72 8763853-4 1996 We examined the induction of p53 and its downstream target, p21WAF1/CIP1, by the microtubule active agents taxol and vinblastine with radiation. Paclitaxel 107-112 tumor protein p53 Homo sapiens 29-32 8763853-5 1996 An increase in induction of both p53 and p21 WAF1/CIP1 was demonstrated when radiation was added to either taxol or vinblastine treatment. Paclitaxel 107-112 tumor protein p53 Homo sapiens 33-36 8521385-2 1995 We examined the ability of three microtubule-active agents, taxol, vinblastine, and nocodazole, to increase p53 levels and activate p53-dependent processes. Paclitaxel 60-65 tumor protein p53 Homo sapiens 108-111 8521385-2 1995 We examined the ability of three microtubule-active agents, taxol, vinblastine, and nocodazole, to increase p53 levels and activate p53-dependent processes. Paclitaxel 60-65 tumor protein p53 Homo sapiens 132-135 33771522-5 2021 PTX increased miR-221-3p expression and regulated MDM2/P53 expression in the PTX-sensitive NSCLC strain (A549). Paclitaxel 0-3 tumor protein p53 Homo sapiens 55-58 7553639-8 1995 Previous depletion of c-raf-1 inhibited both the p21WAF1- and p53-inducing properties of taxol, as well as the activation of MAP kinase. Paclitaxel 89-94 tumor protein p53 Homo sapiens 62-65 7553639-10 1995 Furthermore, the ability of taxol to both induce wild-type p53 in MCF7 cells and activate MAP kinase is also dependent on c-raf-1 expression. Paclitaxel 28-33 tumor protein p53 Homo sapiens 59-62 7553639-0 1995 Taxol induction of p21WAF1 and p53 requires c-raf-1. Paclitaxel 0-5 tumor protein p53 Homo sapiens 31-34 7553639-3 1995 Herein, we show that taxol induced dose- and time-dependent accumulation of the cyclin inhibitor p21WAF1 in both p53 wild-type and p53-null cells, although the degree of induction was greater in cells expressing wild-type p53. Paclitaxel 21-26 tumor protein p53 Homo sapiens 113-116 7553639-3 1995 Herein, we show that taxol induced dose- and time-dependent accumulation of the cyclin inhibitor p21WAF1 in both p53 wild-type and p53-null cells, although the degree of induction was greater in cells expressing wild-type p53. Paclitaxel 21-26 tumor protein p53 Homo sapiens 131-134 7553639-3 1995 Herein, we show that taxol induced dose- and time-dependent accumulation of the cyclin inhibitor p21WAF1 in both p53 wild-type and p53-null cells, although the degree of induction was greater in cells expressing wild-type p53. Paclitaxel 21-26 tumor protein p53 Homo sapiens 131-134 7553639-4 1995 In MCF7 cells, wild-type p53 protein was also induced after taxol treatment, and this induction was mediated primarily by increased protein stability. Paclitaxel 60-65 tumor protein p53 Homo sapiens 25-28 7553639-5 1995 Taxol induced both p21WAF1 and wild-type p53 optimally in MCF7 cells after 20-24-h exposure with an EC50(3) of 5 nM. Paclitaxel 0-5 tumor protein p53 Homo sapiens 41-44 7553639-6 1995 In p53-null PC3M cells, p21WAF1 was similarly induced after 24-h exposure to taxol. Paclitaxel 77-82 tumor protein p53 Homo sapiens 3-6 8521300-8 1995 RESULTS: Within seconds of stimulation, LPS and Taxol induce in Lps(n) macrophages a depression of autophosphorylation, followed within minutes by autophosphorylation of both p53 and p56 lyn species. Paclitaxel 48-53 tumor protein p53 Homo sapiens 175-178 33771522-5 2021 PTX increased miR-221-3p expression and regulated MDM2/P53 expression in the PTX-sensitive NSCLC strain (A549). Paclitaxel 77-80 tumor protein p53 Homo sapiens 55-58 33771522-13 2021 In conclusion, miR-221-3p overexpression could regulate MDM2/p53 signaling pathway to reverse the PTX resistance of NSCLC and induce apoptosis in vitro and vivo. Paclitaxel 98-101 tumor protein p53 Homo sapiens 61-64 34452218-3 2021 This innovative approach explored the great capacity of both polyamidoamine (PAMAM)-paclitaxel (PTX) conjugate and polyethylenimine (PEI) polymers to complex a p53-encoding plasmid DNA (pDNA), highlighting the utility of considering two compacting agents. Paclitaxel 84-94 tumor protein p53 Homo sapiens 160-163 34834551-0 2021 Bioinformatics Analysis Identifies Precision Treatment with Paclitaxel for Hepatocellular Carcinoma Patients Harboring Mutant TP53 or Wild-Type CTNNB1 Gene. Paclitaxel 60-70 tumor protein p53 Homo sapiens 126-130 34834551-7 2021 Accordingly, HCC cell lines harboring mutant TP53 or wild-type CTNNB1 genes are more sensitive to paclitaxel treatment. Paclitaxel 98-108 tumor protein p53 Homo sapiens 45-49 34834551-8 2021 Therefore, our results imply that HCC patients with mutant TP53 or wild-type CTNNB1 genes may benefit from the paclitaxel therapy. Paclitaxel 111-121 tumor protein p53 Homo sapiens 59-63 34799910-0 2021 P1-39: Paclitaxel induces growth inhibition in gefitinib-resistant PC9-MET cells by downregulating MDM2 and activating p53. Paclitaxel 7-17 tumor protein p53 Homo sapiens 119-122 34660779-4 2021 Treatment with PAC and ATRA induced cell cycle arrest at the G2/M phase and apoptosis by upregulating p53 and caspase-8 expression and increased the intracellular calcium (Ca2+) level possibly by enhancing Ca2+ uptake via plasma membrane channels. Paclitaxel 15-18 tumor protein p53 Homo sapiens 102-105 34608124-3 2021 In contrast, bortezomib and paclitaxel could drive U2OS or MG63 toward apoptosis effectively, suggesting that apoptosis induced by bortezomib or paclitaxel is p53-independent. Paclitaxel 145-155 tumor protein p53 Homo sapiens 159-162 34080040-7 2021 All patients with CCNE1 amplification (n = 7), TP53 R175H substitution (n = 6), and RB1 mutation (n = 4) had poor response to paclitaxel plus carboplatin. Paclitaxel 126-136 tumor protein p53 Homo sapiens 47-51 35058503-6 2022 Knockdown of p53, RBL2, or the DREAM component LIN37 increased AURKA/B pathway gene expression and reduced paclitaxel and radiation toxicity in NSCLC cells. Paclitaxel 107-117 tumor protein p53 Homo sapiens 13-16 35566044-9 2022 In contrast, 5 nM Paclitaxel induces TP53 transcription in excess of BCL-2 and Bax. Paclitaxel 18-28 tumor protein p53 Homo sapiens 37-41 35419287-8 2022 The ferroptosis-related p53-SLC7A11-GPX4 pathway was also altered under different treatment propofol, doxorubicin, or paclitaxel regimens. Paclitaxel 118-128 tumor protein p53 Homo sapiens 24-27