PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30760286-0 2019 TOP2A as marker of response to pegylated lyposomal doxorubicin (PLD) in epithelial ovarian cancers. Doxorubicin 51-62 DNA topoisomerase II alpha Homo sapiens 0-5 32599901-10 2020 GADD45A/MYC-silencing and TOP2A-over-expression counteracted the resistance to Dox induced by snoRNAs. Doxorubicin 79-82 DNA topoisomerase II alpha Homo sapiens 26-31 31216997-12 2019 Moreover, flow cytometry suggested TOP2A had anti-apoptotic function, and knockdown of TOP2A could induce resistance to doxorubicin in J82 cells. Doxorubicin 120-131 DNA topoisomerase II alpha Homo sapiens 87-92 26100858-0 2015 TOP2A gene copy gain predicts response of epithelial ovarian cancers to pegylated liposomal doxorubicin: TOP2A as marker of response to PLD in ovarian cancer. Doxorubicin 92-103 DNA topoisomerase II alpha Homo sapiens 0-5 28813519-4 2017 Standard treatment for patients presenting with advanced disease is doxorubicin based chemotherapy which inhibits the actions of the enzyme topoisomerase IIalpha (TOP2A). Doxorubicin 68-79 DNA topoisomerase II alpha Homo sapiens 163-168 28813519-11 2017 Finally, the relation between TOP2A levels and sensitivity for doxorubicin was examined, confirming reports that TOP2A mRNA levels were overexpressed in MPNST and showing that MPNST cell lines exhibited relatively high TOP2A protein levels and sensitivity to doxorubicin. Doxorubicin 63-74 DNA topoisomerase II alpha Homo sapiens 30-35 29728799-4 2018 METHODS: Patients were divided into two groups according to the level of doxorubicin sensitivity marker TOP2a: DOX-Sense and DOX-Res groups. Doxorubicin 73-84 DNA topoisomerase II alpha Homo sapiens 104-109 29728799-7 2018 RESULTS: We found that the average level of TOP2a expression in patients of DOX-Sense group was almost 10 times higher than in patients of DOX-Res group, and the expression of CD68 was 3 times higher in the DOX-Sense group compared to DOX-Res group. Doxorubicin 76-79 DNA topoisomerase II alpha Homo sapiens 44-49 29728799-7 2018 RESULTS: We found that the average level of TOP2a expression in patients of DOX-Sense group was almost 10 times higher than in patients of DOX-Res group, and the expression of CD68 was 3 times higher in the DOX-Sense group compared to DOX-Res group. Doxorubicin 139-142 DNA topoisomerase II alpha Homo sapiens 44-49 29728799-7 2018 RESULTS: We found that the average level of TOP2a expression in patients of DOX-Sense group was almost 10 times higher than in patients of DOX-Res group, and the expression of CD68 was 3 times higher in the DOX-Sense group compared to DOX-Res group. Doxorubicin 139-142 DNA topoisomerase II alpha Homo sapiens 44-49 29728799-7 2018 RESULTS: We found that the average level of TOP2a expression in patients of DOX-Sense group was almost 10 times higher than in patients of DOX-Res group, and the expression of CD68 was 3 times higher in the DOX-Sense group compared to DOX-Res group. Doxorubicin 139-142 DNA topoisomerase II alpha Homo sapiens 44-49 27557643-10 2016 TOP2A knockdown reversed both the anti-tumor effect and significantly reduced DNA damage induced by selinexor/doxorubicin treatment. Doxorubicin 110-121 DNA topoisomerase II alpha Homo sapiens 0-5 24492650-3 2014 This series of events is crucial to elicit the death pathway triggered by doxorubicin and is necessary to promote HuR function in post-transcriptional regulation of gene expression, because genetic ablation of PKCdelta caused the inability of HuR to bind its target mRNAs, topoisomerase IIalpha (TOP2A) included. Doxorubicin 74-85 DNA topoisomerase II alpha Homo sapiens 296-301 25406834-10 2014 DRZ-mediated TOP2A depletion reduced the accumulation of DOX-induced DSB. Doxorubicin 57-60 DNA topoisomerase II alpha Homo sapiens 13-18 21768308-0 2011 Translational control of TOP2A influences doxorubicin efficacy. Doxorubicin 42-53 DNA topoisomerase II alpha Homo sapiens 25-30 24492650-4 2014 In in vitro select doxorubicin-resistant human breast cancer cell lines upregulating the multidrug resistance marker ABCG2, PKCdelta, and HuR proteins were coordinately downregulated together with the doxorubicin target TOP2A protein whose mRNA was HuR-regulated. Doxorubicin 19-30 DNA topoisomerase II alpha Homo sapiens 220-225 24492650-4 2014 In in vitro select doxorubicin-resistant human breast cancer cell lines upregulating the multidrug resistance marker ABCG2, PKCdelta, and HuR proteins were coordinately downregulated together with the doxorubicin target TOP2A protein whose mRNA was HuR-regulated. Doxorubicin 201-212 DNA topoisomerase II alpha Homo sapiens 220-225 24492650-5 2014 Therefore, we show here that PKCdelta, HuR, and TOP2A constitute a network mediating doxorubicin efficacy in breast cancer cells. Doxorubicin 85-96 DNA topoisomerase II alpha Homo sapiens 48-53 21768308-6 2011 In sum, HuR enhances TOP2A translation by competing with miR-548c-3p; their combined actions control TOP2A expression levels and determine the effectiveness of doxorubicin. Doxorubicin 160-171 DNA topoisomerase II alpha Homo sapiens 21-26 19620488-0 2009 Outcome of patients with early-stage breast cancer treated with doxorubicin-based adjuvant chemotherapy as a function of HER2 and TOP2A status. Doxorubicin 64-75 DNA topoisomerase II alpha Homo sapiens 130-135 21188112-1 2010 PURPOSE: Human epidermal growth factor receptor 2 (HER2)/neu, topoisomerase II alpha (TOP2A), and polysomy 17 may predict tumor responsiveness to doxorubicin (DOX) therapy. Doxorubicin 146-157 DNA topoisomerase II alpha Homo sapiens 86-91 19620488-2 2009 We determined the status of the HER2 and TOP2A genes in a large cohort of breast cancer patients treated with adjuvant doxorubicin (A) and cyclophosphamide (C). Doxorubicin 119-130 DNA topoisomerase II alpha Homo sapiens 41-46 19417146-5 2009 Unexpectedly, dexrazoxane was found to cause TOP2A depletion, thereby reducing the doxorubicin-induced accumulation of DSB. Doxorubicin 83-94 DNA topoisomerase II alpha Homo sapiens 45-50 19417146-7 2009 This could be explained by the TOP2A-independent apoptotic effects of each drug: those of doxorubicin included TOP2A-independent DSB formation and depletion of intracellular glutathione, whereas those of dexrazoxane were caspase independent. Doxorubicin 90-101 DNA topoisomerase II alpha Homo sapiens 31-36 19417146-7 2009 This could be explained by the TOP2A-independent apoptotic effects of each drug: those of doxorubicin included TOP2A-independent DSB formation and depletion of intracellular glutathione, whereas those of dexrazoxane were caspase independent. Doxorubicin 90-101 DNA topoisomerase II alpha Homo sapiens 111-116 19417146-8 2009 In conclusion, both doxorubicin and dexrazoxane induce apoptosis via TOP2A-dependent and TOP2A-independent mechanisms, the latter compensating for the reduction in cell killing due to dexrazoxane-induced TOP2A depletion. Doxorubicin 20-31 DNA topoisomerase II alpha Homo sapiens 69-74 19417146-8 2009 In conclusion, both doxorubicin and dexrazoxane induce apoptosis via TOP2A-dependent and TOP2A-independent mechanisms, the latter compensating for the reduction in cell killing due to dexrazoxane-induced TOP2A depletion. Doxorubicin 20-31 DNA topoisomerase II alpha Homo sapiens 89-94 19417146-8 2009 In conclusion, both doxorubicin and dexrazoxane induce apoptosis via TOP2A-dependent and TOP2A-independent mechanisms, the latter compensating for the reduction in cell killing due to dexrazoxane-induced TOP2A depletion. Doxorubicin 20-31 DNA topoisomerase II alpha Homo sapiens 89-94 18574145-4 2008 These experiments identified Top2A expression levels as major determinants of response to the topoisomerase 2 poison doxorubicin and showed that suppression of Top2A produces resistance to doxorubicin in vitro and in vivo. Doxorubicin 117-128 DNA topoisomerase II alpha Homo sapiens 29-34 18574145-4 2008 These experiments identified Top2A expression levels as major determinants of response to the topoisomerase 2 poison doxorubicin and showed that suppression of Top2A produces resistance to doxorubicin in vitro and in vivo. Doxorubicin 117-128 DNA topoisomerase II alpha Homo sapiens 160-165 18574145-4 2008 These experiments identified Top2A expression levels as major determinants of response to the topoisomerase 2 poison doxorubicin and showed that suppression of Top2A produces resistance to doxorubicin in vitro and in vivo. Doxorubicin 189-200 DNA topoisomerase II alpha Homo sapiens 29-34 18574145-4 2008 These experiments identified Top2A expression levels as major determinants of response to the topoisomerase 2 poison doxorubicin and showed that suppression of Top2A produces resistance to doxorubicin in vitro and in vivo. Doxorubicin 189-200 DNA topoisomerase II alpha Homo sapiens 160-165 17089011-6 2006 SK-Br3 cells cultured in the presence of topoisomerase IIalpha (TOP2A) inhibitors doxorubicin and etopoxide (VP-16) demonstrated a 2- to 3-fold increase in FAS promoter activity when compared with control cells growing in drug-free culture conditions. Doxorubicin 82-93 DNA topoisomerase II alpha Homo sapiens 64-69 16935488-1 2006 AIM: To study the predictive role of HER-2 and Topoisomerase IIalpha (TOP2A) in response to primary doxorubicin. Doxorubicin 100-111 DNA topoisomerase II alpha Homo sapiens 70-75 35596703-6 2022 In addition, patients with adverse clinical outcomes were more sensitive to three small molecule inhibitors (bortezomib, doxorubicin, and etoposide), and their targets (PSMB5 and TOP2A) also have elevated expression levels among these patients. Doxorubicin 121-132 DNA topoisomerase II alpha Homo sapiens 179-184 16502015-1 2006 Topoisomerase II-alpha (TOP2A) has been investigated as a potential predictor for the response to doxorubicin-based chemotherapy which is a representative TOP2A inhibitor and one of the most effective chemotherapeutics for the breast cancer treatment. Doxorubicin 98-109 DNA topoisomerase II alpha Homo sapiens 24-29 16502015-1 2006 Topoisomerase II-alpha (TOP2A) has been investigated as a potential predictor for the response to doxorubicin-based chemotherapy which is a representative TOP2A inhibitor and one of the most effective chemotherapeutics for the breast cancer treatment. Doxorubicin 98-109 DNA topoisomerase II alpha Homo sapiens 155-160 16502015-2 2006 We performed the assay for the TOP2A gene amplification and deletion on a tissue microarray (TMA) of 284 breast tumor samples from the patients treated by doxorubicin-based adjuvant chemotherapy. Doxorubicin 155-166 DNA topoisomerase II alpha Homo sapiens 31-36 16502015-9 2006 Our study indicates that response to the doxorubicin-based chemotherapy might be stratified by TOP2A amplification and deletion. Doxorubicin 41-52 DNA topoisomerase II alpha Homo sapiens 95-100 15765123-14 2005 Within the doxorubicin-resistant group, distinct features of candidate genes overexpressions including ABC transporting proteins, solute carriers and TOP2A were suggested. Doxorubicin 11-22 DNA topoisomerase II alpha Homo sapiens 150-155 33904373-7 2021 We were also able to predict several therapeutic drug candidates for sepsis-induced ARDS using Connectivity Map (Cmap) database, among which doxorubicin was identified to interact with TOP2A with a high affinity similar to its endogenous ligand. Doxorubicin 141-152 DNA topoisomerase II alpha Homo sapiens 185-190 33904373-8 2021 Overall, our findings suggest that doxorubicin could be a potential therapeutic for sepsis-induced ARDS by targeting TOP2A, which requires further investigation and validation. Doxorubicin 35-46 DNA topoisomerase II alpha Homo sapiens 117-122 34638362-2 2021 The expression of TOP2A and SIRT1 has implications for the mechanism of action of doxorubicin, which is the backbone of chemotherapy in HR-STS. Doxorubicin 82-93 DNA topoisomerase II alpha Homo sapiens 18-23