PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32456796-0 2020 CD147 promotes DNA damage response and gemcitabine resistance via targeting ATM/ATR/p53 and affects prognosis in pancreatic cancer. gemcitabine 39-50 tumor protein p53 Homo sapiens 84-87 32234756-12 2020 The sensitivity of TP53mut PDAC to gemcitabine in CONKO-001 provides a lead for further mechanistic investigations. gemcitabine 35-46 tumor protein p53 Homo sapiens 19-23 33113997-0 2020 Targeting P53 as a Future Strategy to Overcome Gemcitabine Resistance in Biliary Tract Cancers. gemcitabine 47-58 tumor protein p53 Homo sapiens 10-13 33113997-4 2020 Preclinical studies have demonstrated that p53 mutations in BTCs are associated with enhanced gemcitabine resistance, therefore targeting p53 may be a novel therapeutic strategy for treatment of BTCs. gemcitabine 94-105 tumor protein p53 Homo sapiens 43-46 33113997-4 2020 Preclinical studies have demonstrated that p53 mutations in BTCs are associated with enhanced gemcitabine resistance, therefore targeting p53 may be a novel therapeutic strategy for treatment of BTCs. gemcitabine 94-105 tumor protein p53 Homo sapiens 138-141 32234756-0 2020 TP53 mutations predict sensitivity to adjuvant gemcitabine in patients with pancreatic ductal adenocarcinoma: next-generation sequencing results from the CONKO-001 trial. gemcitabine 47-58 tumor protein p53 Homo sapiens 0-4 32234756-8 2020 In Gem treated patients, TP53 mutations were a positive predictive factor for gemcitabine efficacy (TP53mut: HR for DFS Gem vs Obs: 0.235 (0.130 - 0.423; p<0.001); TP53wt: HR for DFS Gem vs Obs: 0.794 (0.417 - 1.513; p = 0.483) with a significant test for interaction (p=0.003). gemcitabine 78-89 tumor protein p53 Homo sapiens 25-29 32234756-8 2020 In Gem treated patients, TP53 mutations were a positive predictive factor for gemcitabine efficacy (TP53mut: HR for DFS Gem vs Obs: 0.235 (0.130 - 0.423; p<0.001); TP53wt: HR for DFS Gem vs Obs: 0.794 (0.417 - 1.513; p = 0.483) with a significant test for interaction (p=0.003). gemcitabine 78-89 tumor protein p53 Homo sapiens 100-104 32234756-8 2020 In Gem treated patients, TP53 mutations were a positive predictive factor for gemcitabine efficacy (TP53mut: HR for DFS Gem vs Obs: 0.235 (0.130 - 0.423; p<0.001); TP53wt: HR for DFS Gem vs Obs: 0.794 (0.417 - 1.513; p = 0.483) with a significant test for interaction (p=0.003). gemcitabine 78-89 tumor protein p53 Homo sapiens 100-104 32234756-10 2020 CONCLUSION: In CONKO-001, the benefit from adjuvant gemcitabine was confined to the TP53mut patient group. gemcitabine 52-63 tumor protein p53 Homo sapiens 84-88 32456796-5 2020 CD147 knockdown or monoclonal antibodies improved the killing effects of gemcitabine in gemcitabine resistant cells, exhibiting reduced activation of ATM/p53. gemcitabine 73-84 tumor protein p53 Homo sapiens 154-157 32456796-5 2020 CD147 knockdown or monoclonal antibodies improved the killing effects of gemcitabine in gemcitabine resistant cells, exhibiting reduced activation of ATM/p53. gemcitabine 88-99 tumor protein p53 Homo sapiens 154-157 32456796-6 2020 Moreover, we found the interaction of CD147 with ATM, ATR and p53, which was augmented in gemcitabine resistant cells. gemcitabine 90-101 tumor protein p53 Homo sapiens 62-65 30454541-14 2018 Furthermore, Western blot analysis showed that microwave hyperthermia combined with gemcitabine could up-regulate the p53, Caspase-3, Cleaved-Caspase-3, Cleaved-PARP and Bax protein expression. gemcitabine 84-95 tumor protein p53 Homo sapiens 118-121 31871844-8 2019 Three drugs, mitomycin-C, doxorubicin and gemcitabine, were especially more sensitive to bladder cancer with the TP53 mutation. gemcitabine 42-53 tumor protein p53 Homo sapiens 113-117 32427989-7 2020 However, depleting Mdm4 sensitized p53-/- cells to the nucleoside analog gemcitabine, raising the future perspective of using Mdm4 inhibitors as chemosensitizers. gemcitabine 73-84 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. gemcitabine 159-170 tumor protein p53 Homo sapiens 28-32 29783721-0 2018 AZD1775 Increases Sensitivity to Olaparib and Gemcitabine in Cancer Cells with p53 Mutations. gemcitabine 46-57 tumor protein p53 Homo sapiens 79-82 29620279-0 2018 Impact of RUNX2 gene silencing on the gemcitabine sensitivity of p53-mutated pancreatic cancer MiaPaCa-2 spheres. gemcitabine 38-49 tumor protein p53 Homo sapiens 65-68 29620279-2 2018 In the present study, we have demonstrated that, similar to the conventional 2D monolayer culture systems which often lack in vivo physiological insights, RUNX2 gene silencing increases the gemcitabine (GEM) sensitivity of the 3D spheres generated from p53-mutated pancreatic cancer MiaPaCa-2 cells. gemcitabine 190-201 tumor protein p53 Homo sapiens 253-256 29620279-2 2018 In the present study, we have demonstrated that, similar to the conventional 2D monolayer culture systems which often lack in vivo physiological insights, RUNX2 gene silencing increases the gemcitabine (GEM) sensitivity of the 3D spheres generated from p53-mutated pancreatic cancer MiaPaCa-2 cells. gemcitabine 203-206 tumor protein p53 Homo sapiens 253-256 29783721-7 2018 Moreover, the combination of AZD1775 with olaparib or gemcitabine is synergistic in cells with mutant p53 and constitutes a new approach that should be considered in the treatment of advanced and recurrent gynecologic cancer. gemcitabine 54-65 tumor protein p53 Homo sapiens 102-105 29409053-9 2018 Moreover, we observed a synergistic or additive effect of GDC-0575 together with gemcitabine in vitro and in vivo in TP53-proficient but not TP53-deficient sarcoma models. gemcitabine 81-92 tumor protein p53 Homo sapiens 117-121 29788155-14 2018 Among patients treated with GDC-0575 and gemcitabine, there were four confirmed partial responses, three occurring in patients with tumors harboring TP53 mutation. gemcitabine 41-52 tumor protein p53 Homo sapiens 149-153 27888811-3 2017 Overexpression of mutated p53 with reduced or abolished function is often connected to resistance to standard medications, including cisplatin, alkylating agents (temozolomide), anthracyclines, (doxorubicin), antimetabolites (gemcitabine), antiestrogenes (tamoxifen) and EGFR-inhibitors (cetuximab). gemcitabine 226-237 tumor protein p53 Homo sapiens 26-29 28577130-0 2018 Gemcitabine/Cisplatin Treatment Induces Concomitant SERTAD1, CDKN2B and GADD45A Modulation and Cellular Changes in Bladder Cancer Cells Regardless of the Site of TP53 Mutation. gemcitabine 0-11 tumor protein p53 Homo sapiens 162-166 29301826-0 2018 p53-Reactive T Cells Are Associated with Clinical Benefit in Patients with Platinum-Resistant Epithelial Ovarian Cancer After Treatment with a p53 Vaccine and Gemcitabine Chemotherapy. gemcitabine 159-170 tumor protein p53 Homo sapiens 0-3 29115606-3 2018 However, its regulation of chemosensitivity to gemcitabine (GEM) and oxaliplatin (OXA) in p53-deficient PDAC remains unclear. gemcitabine 47-58 tumor protein p53 Homo sapiens 90-93 29115606-3 2018 However, its regulation of chemosensitivity to gemcitabine (GEM) and oxaliplatin (OXA) in p53-deficient PDAC remains unclear. gemcitabine 60-63 tumor protein p53 Homo sapiens 90-93 28854261-13 2017 Gemcitabine-induced uPA promoted invasion, sphere formation and colony formation and attenuated apoptosis induced by gemcitabine in panc-1 CSCs, depending on interaction with mutant p53-R273H. gemcitabine 0-11 tumor protein p53 Homo sapiens 182-185 28854261-13 2017 Gemcitabine-induced uPA promoted invasion, sphere formation and colony formation and attenuated apoptosis induced by gemcitabine in panc-1 CSCs, depending on interaction with mutant p53-R273H. gemcitabine 117-128 tumor protein p53 Homo sapiens 182-185 28854261-15 2017 CONCLUSION: Gemcitabine treatment induced ER stress and promoted mutant p53-R273H stabilization via transcriptionally activated uPA which may contribute to chemoresistance to gemcitabine. gemcitabine 12-23 tumor protein p53 Homo sapiens 72-75 28854261-15 2017 CONCLUSION: Gemcitabine treatment induced ER stress and promoted mutant p53-R273H stabilization via transcriptionally activated uPA which may contribute to chemoresistance to gemcitabine. gemcitabine 175-186 tumor protein p53 Homo sapiens 72-75 28854261-16 2017 Notably, upregulation of uPA by gemcitabine treatment may lead to the failure of CP-31398; thus, a novel strategy for modulating mutant p53 function needs to be developed. gemcitabine 32-43 tumor protein p53 Homo sapiens 136-139 28714514-0 2017 Nuclear expression of Y box binding-1 is important for resistance to chemotherapy including gemcitabine in TP53-mutated bladder cancer. gemcitabine 92-103 tumor protein p53 Homo sapiens 107-111 28714514-10 2017 Nuclear expression of YB-1 is important for resistance to chemotherapy including gemcitabine in TP53-mutated bladder cancer. gemcitabine 81-92 tumor protein p53 Homo sapiens 96-100 28196872-9 2017 Also, MUC16 overexpression induced cisplatin and gemcitabine resistance by downregulation of p53.Conclusions: Our findings indicate a significant role of MUC16 in tumorigenesis and metastasis of lung cancer cells possibly via regulation of TSPYL5 through the JAK2/STAT3/GR axis. gemcitabine 49-60 tumor protein p53 Homo sapiens 93-96 27294865-0 2016 Improvement of gemcitabine sensitivity of p53-mutated pancreatic cancer MiaPaCa-2 cells by RUNX2 depletion-mediated augmentation of TAp73-dependent cell death. gemcitabine 15-26 tumor protein p53 Homo sapiens 42-45 27713122-0 2016 Depletion of pro-oncogenic RUNX2 enhances gemcitabine (GEM) sensitivity of p53-mutated pancreatic cancer Panc-1 cells through the induction of pro-apoptotic TAp63. gemcitabine 42-53 tumor protein p53 Homo sapiens 75-78 27713122-0 2016 Depletion of pro-oncogenic RUNX2 enhances gemcitabine (GEM) sensitivity of p53-mutated pancreatic cancer Panc-1 cells through the induction of pro-apoptotic TAp63. gemcitabine 55-58 tumor protein p53 Homo sapiens 75-78 27713122-1 2016 Recently, we have described that siRNA-mediated silencing of runt-related transcription factor 2 (RUNX2) improves anti-cancer drug gemcitabine (GEM) sensitivity of p53-deficient human pancreatic cancer AsPC-1 cells through the augmentation of p53 family TAp63-dependent cell death pathway. gemcitabine 131-142 tumor protein p53 Homo sapiens 164-167 27713122-1 2016 Recently, we have described that siRNA-mediated silencing of runt-related transcription factor 2 (RUNX2) improves anti-cancer drug gemcitabine (GEM) sensitivity of p53-deficient human pancreatic cancer AsPC-1 cells through the augmentation of p53 family TAp63-dependent cell death pathway. gemcitabine 144-147 tumor protein p53 Homo sapiens 164-167 27713122-9 2016 Taken together, our current observations strongly suggest that depletion of RUNX2 enhances the cytotoxic effect of GEM on p53-mutated Panc-1 cells through the stimulation of TAp63-dependent cell death pathway even in the presence of a large amount of pro-oncogenic mutant p53, and might provide an attractive strategy to treat pancreatic cancer patients with p53 mutations. gemcitabine 115-118 tumor protein p53 Homo sapiens 122-125 27713122-9 2016 Taken together, our current observations strongly suggest that depletion of RUNX2 enhances the cytotoxic effect of GEM on p53-mutated Panc-1 cells through the stimulation of TAp63-dependent cell death pathway even in the presence of a large amount of pro-oncogenic mutant p53, and might provide an attractive strategy to treat pancreatic cancer patients with p53 mutations. gemcitabine 115-118 tumor protein p53 Homo sapiens 272-275 27713122-9 2016 Taken together, our current observations strongly suggest that depletion of RUNX2 enhances the cytotoxic effect of GEM on p53-mutated Panc-1 cells through the stimulation of TAp63-dependent cell death pathway even in the presence of a large amount of pro-oncogenic mutant p53, and might provide an attractive strategy to treat pancreatic cancer patients with p53 mutations. gemcitabine 115-118 tumor protein p53 Homo sapiens 272-275 27461834-0 2016 P53 overexpression and Ki67-index are associated with outcome in ductal pancreatic adenocarcinoma with adjuvant gemcitabine treatment. gemcitabine 112-123 tumor protein p53 Homo sapiens 0-3 27461834-6 2016 However, stratified analysis according to treatment arm revealed that the effect of deregulated p53 expression and high Ki67 expression was restricted to the disease free survival of patients treated with adjuvant gemcitabine. gemcitabine 214-225 tumor protein p53 Homo sapiens 96-99 26606261-0 2015 MicroRNA Profiling Implies New Markers of Gemcitabine Chemoresistance in Mutant p53 Pancreatic Ductal Adenocarcinoma. gemcitabine 42-53 tumor protein p53 Homo sapiens 80-83 26606261-4 2015 METHODS: Gemcitabine-resistant variants of two mutant p53 human PDAC cell lines were established. gemcitabine 9-20 tumor protein p53 Homo sapiens 54-57 26606261-12 2015 CONCLUSION: Consistent miR expression profiles, in part regulated by mutant TP53 gene, were identified in gemcitabine-resistant PDAC with significant MRP-1 and Bcl-2 overexpression. gemcitabine 106-117 tumor protein p53 Homo sapiens 76-80 26427042-5 2015 Gemcitabine was found to be a lytic inducer via activation of the ataxia telangiectasia-mutated (ATM)/p53 genotoxic stress pathway in EBVaGC. gemcitabine 0-11 tumor protein p53 Homo sapiens 102-105 25311384-6 2015 Despite the adverse activation of mutant p53 by gemcitabine, simultaneous treatment of PDAC cells with gemcitabine and p53-reactivating molecules (CP-31398 and RITA) reduced growth rate and induced apoptosis. gemcitabine 103-114 tumor protein p53 Homo sapiens 41-44 25311384-0 2015 Mutant p53 stimulates chemoresistance of pancreatic adenocarcinoma cells to gemcitabine. gemcitabine 76-87 tumor protein p53 Homo sapiens 7-10 26112218-6 2015 Knocking-down of PKM2 significantly enhanced gemcitabine-induced cell apoptosis through the activation of caspase 3/7 and PARP cleavage, and this inhibitory activity was associated with p38-mediated activation of p53 phosphorylation at serine 46. gemcitabine 45-56 tumor protein p53 Homo sapiens 213-216 26028101-5 2015 Meanwhile, it could also significantly decrease gemcitabine-induced increase of transcellular and paracellular leak, ROS level, PARP-1 activity, Act-MMP9 level, mRNA expressions of p53 and Rac-1, expression of PARP-1 and apoptosis rate (p<0.01). gemcitabine 48-59 tumor protein p53 Homo sapiens 181-184 25311384-10 2015 Together, our results show that gemcitabine aberrantly stimulates mutant p53 activity in PDAC cells identifying key processes with potential for therapeutic targeting. gemcitabine 32-43 tumor protein p53 Homo sapiens 73-76 25311384-3 2015 The purpose of this study was to assess the relevance of the p53 status on the PDAC cells response to the standard drug gemcitabine. gemcitabine 120-131 tumor protein p53 Homo sapiens 61-64 25311384-5 2015 We showed that gemcitabine stabilized mutant p53 protein in the nuclei and induced chemoresistance, concurrent with the mutant p53-dependent expression of Cdk1 and CCNB1 genes, resulting in a hyperproliferation effect. gemcitabine 15-26 tumor protein p53 Homo sapiens 45-48 25311384-5 2015 We showed that gemcitabine stabilized mutant p53 protein in the nuclei and induced chemoresistance, concurrent with the mutant p53-dependent expression of Cdk1 and CCNB1 genes, resulting in a hyperproliferation effect. gemcitabine 15-26 tumor protein p53 Homo sapiens 127-130 25311384-6 2015 Despite the adverse activation of mutant p53 by gemcitabine, simultaneous treatment of PDAC cells with gemcitabine and p53-reactivating molecules (CP-31398 and RITA) reduced growth rate and induced apoptosis. gemcitabine 48-59 tumor protein p53 Homo sapiens 41-44 26642705-10 2015 Treatment with AdCMVE2F-1 plus gemcitabine enhanced endogenous p53 expression in LoVo cells, which contain wild-type p53; however, the finding that the synergistic effect can also be observed in mutant p53-expressing SW620 and DLD-1 cells suggests that wild-type p53 function may not be necessary for the therapeutic effects of this drug combination. gemcitabine 31-42 tumor protein p53 Homo sapiens 63-66 26642705-10 2015 Treatment with AdCMVE2F-1 plus gemcitabine enhanced endogenous p53 expression in LoVo cells, which contain wild-type p53; however, the finding that the synergistic effect can also be observed in mutant p53-expressing SW620 and DLD-1 cells suggests that wild-type p53 function may not be necessary for the therapeutic effects of this drug combination. gemcitabine 31-42 tumor protein p53 Homo sapiens 117-120 26642705-10 2015 Treatment with AdCMVE2F-1 plus gemcitabine enhanced endogenous p53 expression in LoVo cells, which contain wild-type p53; however, the finding that the synergistic effect can also be observed in mutant p53-expressing SW620 and DLD-1 cells suggests that wild-type p53 function may not be necessary for the therapeutic effects of this drug combination. gemcitabine 31-42 tumor protein p53 Homo sapiens 117-120 26642705-10 2015 Treatment with AdCMVE2F-1 plus gemcitabine enhanced endogenous p53 expression in LoVo cells, which contain wild-type p53; however, the finding that the synergistic effect can also be observed in mutant p53-expressing SW620 and DLD-1 cells suggests that wild-type p53 function may not be necessary for the therapeutic effects of this drug combination. gemcitabine 31-42 tumor protein p53 Homo sapiens 117-120 24996846-8 2014 Induction of gammaH2AX levels was chemotherapeutic dependent and correlated closely with potentiation of gemcitabine and camptothecin in p53 mutant colon cancer cells. gemcitabine 105-116 tumor protein p53 Homo sapiens 137-140 25349305-4 2015 We hypothesized that combined CDKN1A-TP53 loss would make bladder cancer sensitive to combined treatment with gemcitabine and Chk1 inhibitor. gemcitabine 110-121 tumor protein p53 Homo sapiens 37-41 25349305-5 2015 Here, we show that TP53-CDKN1A double-mutant bladder cancer cell lines, 647V and RT-112, have a remarkable increase in p-Chk1 levels and G2-M arrest in response to gemcitabine treatment, with a heightened sensitivity to combination treatment with gemcitabine and either Chk1 inhibitor PF477736 or AZD7762, in comparison with other bladder cancer cell lines (either TP53 or p21 deficient). gemcitabine 164-175 tumor protein p53 Homo sapiens 19-23 25349305-5 2015 Here, we show that TP53-CDKN1A double-mutant bladder cancer cell lines, 647V and RT-112, have a remarkable increase in p-Chk1 levels and G2-M arrest in response to gemcitabine treatment, with a heightened sensitivity to combination treatment with gemcitabine and either Chk1 inhibitor PF477736 or AZD7762, in comparison with other bladder cancer cell lines (either TP53 or p21 deficient). gemcitabine 164-175 tumor protein p53 Homo sapiens 365-369 25349305-5 2015 Here, we show that TP53-CDKN1A double-mutant bladder cancer cell lines, 647V and RT-112, have a remarkable increase in p-Chk1 levels and G2-M arrest in response to gemcitabine treatment, with a heightened sensitivity to combination treatment with gemcitabine and either Chk1 inhibitor PF477736 or AZD7762, in comparison with other bladder cancer cell lines (either TP53 or p21 deficient). gemcitabine 247-258 tumor protein p53 Homo sapiens 19-23 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. gemcitabine 178-189 tumor protein p53 Homo sapiens 115-118 22903553-12 2012 Taken together, these results provide evidence that sMEK1 can effectively regulate the pro-apoptotic activity of gemcitabine through the up-regulation of p53 expression. gemcitabine 113-124 tumor protein p53 Homo sapiens 154-157 24804820-8 2014 Furthermore, as shown by our results, the inhibition of gemcitabine-induced autophagy by chloroquine shifts the expression of the p53 protein, Bcl-2 family proteins and the relative Bax/Bcl-xL ratio in favor of promoting apoptosis. gemcitabine 56-67 tumor protein p53 Homo sapiens 130-133 24114124-10 2014 Consistent with abrogation of the Chk1 and p53-dependent G2/M checkpoint, mutant TP53 HT-29 colon cancer cells were more sensitive to gemcitabine when also treated with LY2603618, while wild-type TP53 HCT116 cells were not sensitized by LY2603618 to gemcitabine. gemcitabine 250-261 tumor protein p53 Homo sapiens 81-85 24114124-11 2014 Treatment of Calu-6 human mutant TP53 lung cancer cell xenografts with gemcitabine resulted in a stimulation of Chk1 kinase activity that was inhibited by co-administration of LY2603618. gemcitabine 71-82 tumor protein p53 Homo sapiens 33-37 23881403-8 2013 Meanwhile, Numb knockdown increased chemoresistance but decreased activated p53 and cleaved-caspase-3 protein expression in gemcitabine-treated Capan-2 cells. gemcitabine 124-135 tumor protein p53 Homo sapiens 76-79 23579097-6 2013 The combined treatment with BLU and gemcitabine further activated p53 and p21 expression, whereas the productions of Bcl-2, Bcl-xL, and nuclear factor-kappa B proteins were decreased, with BLU possibly being more effective in the treatment of ovarian cancer when given in combination with gemcitabine, rather than as a single agent. gemcitabine 36-47 tumor protein p53 Homo sapiens 66-69 23053941-0 2012 Toxicogenomic activity of gemcitabine in two TP53-mutated bladder cancer cell lines: special focus on cell cycle-related genes. gemcitabine 26-37 tumor protein p53 Homo sapiens 45-49 23053941-7 2012 Gemcitabine had distinct toxicogenomic effects in the bladder transitional carcinoma cell lines with two different TP53 mutations. gemcitabine 0-11 tumor protein p53 Homo sapiens 115-119 22903553-10 2012 The p53 and p21 promoter luciferase activities were promoted by either sMEK1 or gemcitabine, and sMEK1 and gemcitabine combined additively activated the promoter further. gemcitabine 80-91 tumor protein p53 Homo sapiens 4-7 22903553-10 2012 The p53 and p21 promoter luciferase activities were promoted by either sMEK1 or gemcitabine, and sMEK1 and gemcitabine combined additively activated the promoter further. gemcitabine 107-118 tumor protein p53 Homo sapiens 4-7 24114124-10 2014 Consistent with abrogation of the Chk1 and p53-dependent G2/M checkpoint, mutant TP53 HT-29 colon cancer cells were more sensitive to gemcitabine when also treated with LY2603618, while wild-type TP53 HCT116 cells were not sensitized by LY2603618 to gemcitabine. gemcitabine 134-145 tumor protein p53 Homo sapiens 81-85 24507760-3 2014 METHOD: We have developed a redox-responsive thiolated gelatin based nanoparticle system that efficiently delivers its payload in the presence of glutathione-mediated reducing intra-cellular environment and could be successfully used for site-specific wt-p53 expressing plasmid DNA as well as gemcitabine delivery by targeting epidermal growth factor receptor (EGFR). gemcitabine 293-304 tumor protein p53 Homo sapiens 255-258 23648290-7 2013 Exposure of MM cells to [Gem+Clo] also decreased the level of ribosomal RNA (rRNA), which might have resulted in nucleolar stress, as reported previously, and caused a p53-dependent cell death. gemcitabine 25-28 tumor protein p53 Homo sapiens 168-171 23648290-8 2013 A reduction by approximately 50% in the cytotoxicity of Gem and Clo was observed in the presence of pifithrin alpha, a p53 inhibitor. gemcitabine 56-59 tumor protein p53 Homo sapiens 119-122 23579097-8 2013 Taken together, our results provide evidence that BLU can effectively regulate the pro-apoptotic and anti-angiogenic activity of gemcitabine through the direct interaction with vascular endothelial growth factor receptor-2, as well as the up-regulation of p21 and p53 expression. gemcitabine 129-140 tumor protein p53 Homo sapiens 264-267 23520471-8 2013 Additionally, MK1775 significantly enhances the cytotoxic effect of gemcitabine in sarcoma cells lines with different p53 mutational status. gemcitabine 68-79 tumor protein p53 Homo sapiens 118-121 22353361-0 2012 Involvement of p53 in gemcitabine mediated cytotoxicity and radiosensitivity in breast cancer cell lines. gemcitabine 22-33 tumor protein p53 Homo sapiens 15-18 22710877-7 2012 Tumors from nude mice injected with BxPC-3 PaCa cells and treated with a combination of oridonin and gemcitabine showed a significant upregulation in p38 and p53 activation (P<0.05 vs. control, P<0.05 vs. gemcitabine or oridonin alone). gemcitabine 101-112 tumor protein p53 Homo sapiens 158-161 22710877-8 2012 Taken together, our results demonstrate that oridonin can potentiate the effects of gemcitabine in PaCa through the mitogen-activated protein kinase (MAPK)-p38 signaling pathway, which is dependent on p53 activation. gemcitabine 84-95 tumor protein p53 Homo sapiens 201-204 22353361-9 2012 dFdCyd combined with radiation reduces the efficacy of chemo-radiotherapy in p53 mutated cells. gemcitabine 0-6 tumor protein p53 Homo sapiens 77-80 22353361-10 2012 Therefore, p53-mutated cancer could be a counter-indication for radiation-gemcitabine combined treatment. gemcitabine 74-85 tumor protein p53 Homo sapiens 11-14 21489314-16 2011 The inverse effect was observed in the TP53 mutated T24 cell line where TFAP2alpha silencing augmented cisplatin and gemcitabine sensitivity and did not stimulate proliferation. gemcitabine 117-128 tumor protein p53 Homo sapiens 39-43 22041920-11 2012 Among these changes, RT-PCR and Western blotting showed that expression of tumor protein 53-induced nuclear protein 1, a gene regulating cell death and DNA repair, was increased by gemcitabine treatment and substantially decreased by GSK3beta inhibition. gemcitabine 181-192 tumor protein p53 Homo sapiens 75-91 21377279-0 2011 Retention of the in vitro radiosensitizing potential of gemcitabine under anoxic conditions, in p53 wild-type and p53-deficient non-small-cell lung carcinoma cells. gemcitabine 56-67 tumor protein p53 Homo sapiens 96-99 21377279-9 2011 Although radiosensitization was observed in both p53 wild-type and p53-deficient cells, p53 status might influence induction of apoptosis after gemcitabine/radiation treatment, whereas no effect on cell cycle progression was noticed. gemcitabine 144-155 tumor protein p53 Homo sapiens 67-70 21377279-9 2011 Although radiosensitization was observed in both p53 wild-type and p53-deficient cells, p53 status might influence induction of apoptosis after gemcitabine/radiation treatment, whereas no effect on cell cycle progression was noticed. gemcitabine 144-155 tumor protein p53 Homo sapiens 67-70 20480521-13 2010 However, gemcitabine and dicoumarol combination induced increased p53 and decreased Bcl-(XL) levels in KKU-100, but not in KKU-M214 cells. gemcitabine 9-20 tumor protein p53 Homo sapiens 66-69 20976259-7 2010 Cell lines with truncation, deletion, and null status of p53 were resistant to gemcitabine without apparent relationship to RRM1 levels. gemcitabine 79-90 tumor protein p53 Homo sapiens 57-60 20976259-9 2010 The impact of p53 mutations in patients treated with gemcitabine should be studied in prospective clinical trials to develop a model with improved precision of predicting drug efficacy. gemcitabine 53-64 tumor protein p53 Homo sapiens 14-17 20558835-0 2010 Cell cycle arrest and apoptosis in TP53 subtypes of bladder carcinoma cell lines treated with cisplatin and gemcitabine. gemcitabine 108-119 tumor protein p53 Homo sapiens 35-39 20558835-8 2010 TP53-wild type cells (RT4) were more sensitive to apoptosis than were mutated TP53 cells when treated with cisplatin or gemcitabine. gemcitabine 120-131 tumor protein p53 Homo sapiens 0-4 20558835-8 2010 TP53-wild type cells (RT4) were more sensitive to apoptosis than were mutated TP53 cells when treated with cisplatin or gemcitabine. gemcitabine 120-131 tumor protein p53 Homo sapiens 78-82 20422343-12 2010 Our data provide evidence that p73 might compensate for p53 function in gemcitabine-induced apoptosis of HuCCT1 cells. gemcitabine 72-83 tumor protein p53 Homo sapiens 56-59 20053762-7 2010 This compound abrogates an etoposide-induced G(2) arrest with an IC(50) of 55 nmol/L in HT29 cells, and significantly enhances the cell killing of gemcitabine and SN38 by 3.0- to 29-fold in several colon tumor lines in vitro and in a p53-dependent fashion. gemcitabine 147-158 tumor protein p53 Homo sapiens 234-237 19887545-6 2009 MK-1775 abrogates G(2) DNA damage checkpoint, leading to apoptosis in combination with DNA-damaging chemotherapeutic agents such as gemcitabine, carboplatin, and cisplatin selectively in p53-deficient cells. gemcitabine 132-143 tumor protein p53 Homo sapiens 187-190 16690105-7 2006 In the gemcitabine plus cisplatin treatment arm compared to either alone, there was also downregulation of MSH2, p53, and ERCC1 expression. gemcitabine 7-18 tumor protein p53 Homo sapiens 113-116 17079445-5 2006 In contrast, isogenic cells lacking functional p53 continued to enter S phase regardless of nutlin-3 pretreatment and remained highly susceptible to gemcitabine-mediated cytotoxicity. gemcitabine 149-160 tumor protein p53 Homo sapiens 47-50 17079445-6 2006 The sequential treatment with nutlin-3 alone, followed by transient exposure to nutlin-3 plus gemcitabine, efficiently compromised the clonogenicity of tumor cells with deletions or mutations of p53 but largely spared the proliferation of nontransformed human keratinocytes. gemcitabine 94-105 tumor protein p53 Homo sapiens 195-198 21479491-4 2008 Two representative chemotherapeutic agents for pancreatic cancer, 5-fluorouracil and gemcitabine, promoted cell death in a p53-dependent manner; however, 1% hypoxia caused chemoresistance to these drugs. gemcitabine 85-96 tumor protein p53 Homo sapiens 123-126 18690840-11 2008 This retrospective study indicates that FHIT-/p53+ status might be a biological variable influencing the efficacy of carboplatin/gemcitabine treatment in NSCLC. gemcitabine 129-140 tumor protein p53 Homo sapiens 46-49 17671697-7 2007 In addition, the gemcitabine pretreatment up-regulated DR-5 and p53 protein expression in a time-dependent manner, which suggests the possible involvement of the p53 protein as a transcriptional factor for DR-5 up-regulation. gemcitabine 17-28 tumor protein p53 Homo sapiens 64-67 17671697-7 2007 In addition, the gemcitabine pretreatment up-regulated DR-5 and p53 protein expression in a time-dependent manner, which suggests the possible involvement of the p53 protein as a transcriptional factor for DR-5 up-regulation. gemcitabine 17-28 tumor protein p53 Homo sapiens 162-165 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. gemcitabine 0-11 tumor protein p53 Homo sapiens 170-173 15464472-13 2004 Combined gemcitabine and bortezomib enhanced p21 and p53 expression and induced S-phase and G2/M cell-cycle arrests, respectively. gemcitabine 9-20 tumor protein p53 Homo sapiens 53-56 16505115-1 2006 Nucleoside anticancer drugs like gemcitabine (2"-deoxy-2",2"-difluorocytidine) are potent inducers of p53, and ectopic expression of wild-type p53 sensitizes cells to these agents. gemcitabine 33-44 tumor protein p53 Homo sapiens 102-105 16505115-1 2006 Nucleoside anticancer drugs like gemcitabine (2"-deoxy-2",2"-difluorocytidine) are potent inducers of p53, and ectopic expression of wild-type p53 sensitizes cells to these agents. gemcitabine 33-44 tumor protein p53 Homo sapiens 143-146 16505115-1 2006 Nucleoside anticancer drugs like gemcitabine (2"-deoxy-2",2"-difluorocytidine) are potent inducers of p53, and ectopic expression of wild-type p53 sensitizes cells to these agents. gemcitabine 46-77 tumor protein p53 Homo sapiens 102-105 16505115-1 2006 Nucleoside anticancer drugs like gemcitabine (2"-deoxy-2",2"-difluorocytidine) are potent inducers of p53, and ectopic expression of wild-type p53 sensitizes cells to these agents. gemcitabine 46-77 tumor protein p53 Homo sapiens 143-146 16505115-5 2006 T-ara-C and gemcitabine markedly induced p53 accumulation as well as increased levels of phospho-p53 (Ser15/Ser20/Ser46) and induced its binding to a consensus p53 response element. gemcitabine 12-23 tumor protein p53 Homo sapiens 41-44 16505115-5 2006 T-ara-C and gemcitabine markedly induced p53 accumulation as well as increased levels of phospho-p53 (Ser15/Ser20/Ser46) and induced its binding to a consensus p53 response element. gemcitabine 12-23 tumor protein p53 Homo sapiens 97-100 16505115-5 2006 T-ara-C and gemcitabine markedly induced p53 accumulation as well as increased levels of phospho-p53 (Ser15/Ser20/Ser46) and induced its binding to a consensus p53 response element. gemcitabine 12-23 tumor protein p53 Homo sapiens 97-100 16505115-6 2006 Despite robust activation of p53 by T-ara-C and gemcitabine, we found that wild-type and p53-/- HCT 116 cells exhibited almost equivalent sensitivity towards these nucleosides. gemcitabine 48-59 tumor protein p53 Homo sapiens 29-32 16505115-7 2006 Examination of p73 revealed that T-ara-C and gemcitabine markedly increased p73 protein levels and p73 DNA-binding activities in both p53-/- and wild-type cells. gemcitabine 45-56 tumor protein p53 Homo sapiens 134-137 16505115-10 2006 HCT 116 lines, wherein the downstream p53/p73 targets Bax and PUMA (p53 up-regulated modulator of apoptosis) were deleted, were less sensitive to T-ara-C and gemcitabine. gemcitabine 158-169 tumor protein p53 Homo sapiens 38-41 16505115-10 2006 HCT 116 lines, wherein the downstream p53/p73 targets Bax and PUMA (p53 up-regulated modulator of apoptosis) were deleted, were less sensitive to T-ara-C and gemcitabine. gemcitabine 158-169 tumor protein p53 Homo sapiens 68-71 16006755-0 2005 Enhancement of gemcitabine-induced apoptosis by restoration of p53 function in human pancreatic tumors. gemcitabine 15-26 tumor protein p53 Homo sapiens 63-66 16006755-7 2005 Moreover, the chemosensitization observed in tumors treated with the combination gemcitabine-p53 correlated with differential histological features such as important increases in intratumoral fibrosis and apoptotic levels, when compared with unimodal treatments. gemcitabine 81-92 tumor protein p53 Homo sapiens 93-96 16006755-8 2005 Taken together, our data indicate that reintroduction of p53 function in human pancreatic tumors in vivo allows to restore molecular pathways improving the response to gemcitabine. gemcitabine 168-179 tumor protein p53 Homo sapiens 57-60 16238441-3 2005 In the present study, we investigated the role of TP53 in the radiosensitizing effect of gemcitabine. gemcitabine 89-100 tumor protein p53 Homo sapiens 50-54 15476743-0 2004 Extracellular signal-regulated kinase activation and Bcl-2 downregulation mediate apoptosis after gemcitabine treatment partly via a p53-independent pathway. gemcitabine 98-109 tumor protein p53 Homo sapiens 133-136 15476743-3 2004 We studied the molecular mechanisms of gemcitabine-induced apoptosis and determined the role of p53 function on the cytotoxic effects of gemcitabine in human nonsmall cell lung cancer (NSCLC) H1299 and H1299/p53 cells. gemcitabine 137-148 tumor protein p53 Homo sapiens 96-99 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. gemcitabine 330-341 tumor protein p53 Homo sapiens 35-38 15199526-2 2004 In breast cancer cell lines that expressed either wild-type p53 (MCF-7) or mutant p53 (MCF-7/Adr), sensitivity to the cytotoxic effects of gemcitabine during a 24-hour incubation was similar (IC(50) values 80 and 60 nmol/L in MCF-7 and MCF-7/Adr, respectively). gemcitabine 139-150 tumor protein p53 Homo sapiens 60-63 15199526-2 2004 In breast cancer cell lines that expressed either wild-type p53 (MCF-7) or mutant p53 (MCF-7/Adr), sensitivity to the cytotoxic effects of gemcitabine during a 24-hour incubation was similar (IC(50) values 80 and 60 nmol/L in MCF-7 and MCF-7/Adr, respectively). gemcitabine 139-150 tumor protein p53 Homo sapiens 82-85 12811511-10 2003 There was a significant upregulation of p53, p21(waf1), and p27 in MCF7 and MCF-10A cells treated with the combination of gemcitabine and BRYO compared to gemcitabine-treated cells. gemcitabine 122-133 tumor protein p53 Homo sapiens 40-43 11802204-0 2002 Expression of a non-functional p53 affects the sensitivity of cancer cells to gemcitabine. gemcitabine 78-89 tumor protein p53 Homo sapiens 31-34 12597983-0 2003 Preclinical evaluation of a radiosensitizing effect of gemcitabine in p53 mutant and p53 wild type bladder cancer cells. gemcitabine 55-66 tumor protein p53 Homo sapiens 70-73 11802204-3 2002 The present study was performed to gain insight into the role of p53 status on the cytotoxicity of gemcitabine on cancer cells. gemcitabine 99-110 tumor protein p53 Homo sapiens 65-68 11802204-11 2002 This corresponded with suppression of Bcl-2 and Bcl-X/L expression in wt-p53 cells exposed to gemcitabine whereas Bcl-2 levels remained stable and Bcl-X/L levels increased in mut-p53 cells exposed to gemcitabine. gemcitabine 94-105 tumor protein p53 Homo sapiens 73-76 11489842-0 2001 Radiosensitization by gemcitabine in p53 wild-type and mutant MCF-7 breast carcinoma cell lines. gemcitabine 22-33 tumor protein p53 Homo sapiens 37-40 11802204-12 2002 We conclude that the p53 status of cancer cells influences their sensitivity to gemcitabine cytotoxicity. gemcitabine 80-91 tumor protein p53 Homo sapiens 21-24 11802204-13 2002 Our evidence suggests that loss of p53 function leads to loss of cell cycle control and alterations in the apoptotic cascade, conferring resistance to gemcitabine in cancer cell lines displaying a mut-p53. gemcitabine 151-162 tumor protein p53 Homo sapiens 35-38 11802204-13 2002 Our evidence suggests that loss of p53 function leads to loss of cell cycle control and alterations in the apoptotic cascade, conferring resistance to gemcitabine in cancer cell lines displaying a mut-p53. gemcitabine 151-162 tumor protein p53 Homo sapiens 201-204 11585734-2 2001 Here we show that E2F1 in combination with the most clinically efficient drug, gemcitabine, resulted in a strong induction of apoptosis independent of functional p53, whereas the effect of either therapy alone varied between different cell lines. gemcitabine 79-90 tumor protein p53 Homo sapiens 162-165 11751391-3 2001 Here, we report that the DNA-dependent protein kinase (DNA-PK) and p53 are able to form a protein complex that interacts with the gemcitabine-containing DNA and plays a role in signaling to apoptotic pathways. gemcitabine 130-141 tumor protein p53 Homo sapiens 67-70 11751391-4 2001 DNA-PK/Ku and p53 were copurified in a protein fraction that binds to gemcitabine-containing DNA in preference to normal DNA. gemcitabine 70-81 tumor protein p53 Homo sapiens 14-17 11751391-6 2001 Treatment with gemcitabine resulted in an increase of DNA-PK and p53 protein and an increase in the phosphorylation of p53 at Ser15. gemcitabine 15-26 tumor protein p53 Homo sapiens 65-68 11751391-6 2001 Treatment with gemcitabine resulted in an increase of DNA-PK and p53 protein and an increase in the phosphorylation of p53 at Ser15. gemcitabine 15-26 tumor protein p53 Homo sapiens 119-122 11751391-7 2001 Furthermore, confocal microscopy demonstrated a colocalization of DNA-PK and p53 to the nucleus in cells treated with gemcitabine. gemcitabine 118-129 tumor protein p53 Homo sapiens 77-80 11751391-9 2001 Although the wild-type p53 present in the protein complex exhibited 3"-5" exonuclease activity, it was incapable of excising the incorporated gemcitabine from DNA. gemcitabine 142-153 tumor protein p53 Homo sapiens 23-26 11489842-9 2001 These results demonstrate that a wild-type p53 cell line can be radiosensitized by dFdCyd, presumably because it was able to deplete dATP levels and progress through the cell cycle for at least 24 h after drug and radiation treatment. gemcitabine 83-89 tumor protein p53 Homo sapiens 43-46 11458051-0 2001 Functional p53 mutation as a molecular determinant of paclitaxel and gemcitabine susceptibility in human bladder cancer. gemcitabine 69-80 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. gemcitabine 66-77 tumor protein p53 Homo sapiens 34-37 34959348-0 2021 Modified Gold Nanoparticles to Overcome the Chemoresistance to Gemcitabine in Mutant p53 Cancer Cells. gemcitabine 63-74 tumor protein p53 Homo sapiens 85-88 11085531-12 2000 After a 24 h incubation with dFdCyd alone or in combination with ionizing radiation, U251 cells readily accumulated in S-phase, which remained elevated for at least 72 h, consistent with previous results in other mutant p53 cell lines. gemcitabine 29-35 tumor protein p53 Homo sapiens 220-223 11085531-16 2000 These results suggest that the G1 block in D54 cells resulting from wild-type p53 induction prevented radiosensitization by dFdCyd. gemcitabine 124-130 tumor protein p53 Homo sapiens 78-81 9772293-7 1998 The accumulated p53 was biochemically active, as measured in a transient transfection assay upon treatment with gemcitabine, cisplatin, etoposide, and Taxol. gemcitabine 112-123 tumor protein p53 Homo sapiens 16-19 10811472-5 2000 Although wt-p53 transduction before drug treatment induced chemoresistance, p53 transduction in cells treated previously with gemcitabine increased cytotoxicity. gemcitabine 126-137 tumor protein p53 Homo sapiens 76-79 10803919-0 2000 The role of p53 in gemcitabine-mediated cytotoxicity and radiosensitization. gemcitabine 19-30 tumor protein p53 Homo sapiens 12-15 10803919-1 2000 PURPOSE: We compared the cytotoxic and radiosensitizing effects of gemcitabine (2",2"-difluoro-2"-deoxycytidine, dFdCyd), a clinically valuable radiosensitizer, in colon cancer RKO cells which differed in their p53 status. gemcitabine 67-78 tumor protein p53 Homo sapiens 211-214 10803919-5 2000 The cytotoxic effect of dFdCyd in RKO-P cells was accompanied by induction of the proapoptotic protein Bax at the time when p53 was induced. gemcitabine 24-30 tumor protein p53 Homo sapiens 124-127 10803919-6 2000 In contrast, similar treatment of RKO-E6 cells with dFdCyd resulted in only limited expression of Bax, suggesting that the cytotoxic effect of dFdCyd was mediated, in part, by a p53-dependent apoptosis pathway. gemcitabine 52-58 tumor protein p53 Homo sapiens 178-181 10803919-6 2000 In contrast, similar treatment of RKO-E6 cells with dFdCyd resulted in only limited expression of Bax, suggesting that the cytotoxic effect of dFdCyd was mediated, in part, by a p53-dependent apoptosis pathway. gemcitabine 143-149 tumor protein p53 Homo sapiens 178-181 10803919-11 2000 CONCLUSION: These results suggest that p53 status may influence dFdCyd-mediated apoptosis, cytotoxicity, and cell cycle progression but do not support an important role for p53 in radiosensitization. gemcitabine 64-70 tumor protein p53 Homo sapiens 39-42 10341297-3 1999 In this study, we investigated the molecular mechanisms by which auristatin-PE, a newly developed experimental agent, and gemcitabine, a commercially available anti-cancer agent, exert their inhibitory effects on pancreatic cancer cell lines containing wild-type p53 (HPAC) and mutant p53 (PANC-1). gemcitabine 122-133 tumor protein p53 Homo sapiens 263-266 34959348-7 2021 The nanostructures generated here provide a non-toxic and powerful system for the delivery of gapmers in cancer cells, which significantly downregulated mutant p53 proteins and altered molecular markers related to cell growth and apoptosis, thus overcoming chemoresistance to gemcitabine. gemcitabine 276-287 tumor protein p53 Homo sapiens 160-163 34781244-2 2021 Gemcitabine (GEM) is the first-line treatment for PDAC, but its efficacy is limited in most patients due to the GEM resistance from KRAS and P53 gene mutations. gemcitabine 0-11 tumor protein p53 Homo sapiens 141-144 34781244-2 2021 Gemcitabine (GEM) is the first-line treatment for PDAC, but its efficacy is limited in most patients due to the GEM resistance from KRAS and P53 gene mutations. gemcitabine 13-16 tumor protein p53 Homo sapiens 141-144