PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 12684687-5 2003 The increased growth inhibition to doxorubicin after loss of Brca1 correlated with increased cell killing caused by increased apoptosis. Doxorubicin 35-46 BRCA1 DNA repair associated Homo sapiens 61-66 17492376-6 2008 Six of the 15 BRCA1 carrier women given docetaxel with doxorubicin responded (complete or partial), compared to 29 of 29 given other (DNA-damaging) therapies (P=0.001). Doxorubicin 55-66 BRCA1 DNA repair associated Homo sapiens 14-19 15607317-4 2005 The method was applied to study the alteration of BRCA1 gene expression after exposure to taxol, doxorubicin, 5-fluorouracil, etoposide or gamma irradiation in human MCF-7 breast cancer cells. Doxorubicin 97-108 BRCA1 DNA repair associated Homo sapiens 50-55 12698198-9 2003 BRCA1 reconstitution reverted the hypersensitivity to CDDP (P<0.02), and restored the sensitivity to Dox (P<0.05) and Tax (P<0.001), compared with parental HCC1937 cells. Doxorubicin 104-107 BRCA1 DNA repair associated Homo sapiens 0-5 35242827-1 2022 Objective: Animal models suggest that BRCA1/2 mutations increase doxorubicin-induced cardiotoxicity risk but data in humans are limited. Doxorubicin 65-76 BRCA1 DNA repair associated Homo sapiens 38-45 12024039-7 2002 BRCA1 also conferred diminished cell death in a p53-dependent manner in response to adriamycin compared to that conferred by controls. Doxorubicin 84-94 BRCA1 DNA repair associated Homo sapiens 0-5 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. Doxorubicin 67-77 BRCA1 DNA repair associated Homo sapiens 14-19 10884389-2 2000 In this study, we show that BRCA1 is initially up-regulated, followed by a reduction to below basal levels in response to treatment with the DNA-damaging agents adriamycin and mitomycin C, and that the reduction of BRCA1 expression is dependent on the presence of wild-type p53. Doxorubicin 161-171 BRCA1 DNA repair associated Homo sapiens 28-33 10884389-2 2000 In this study, we show that BRCA1 is initially up-regulated, followed by a reduction to below basal levels in response to treatment with the DNA-damaging agents adriamycin and mitomycin C, and that the reduction of BRCA1 expression is dependent on the presence of wild-type p53. Doxorubicin 161-171 BRCA1 DNA repair associated Homo sapiens 215-220 10884389-5 2000 ATM(-)(/-) lymphoblastoid cells were deficient in their ability to reduce BRCA1 protein in response to DNA damage, whereas the wild-type counterparts reduced BRCA1 protein levels after exposure to adriamycin. Doxorubicin 197-207 BRCA1 DNA repair associated Homo sapiens 158-163 10196224-6 1999 The association of BRCA1 with CtIP was also abrogated in cells treated with DNA-damaging agents including UV, gamma-irradiation, and adriamycin, a response correlated with BRCA1 phosphorylation. Doxorubicin 133-143 BRCA1 DNA repair associated Homo sapiens 19-24 10196224-6 1999 The association of BRCA1 with CtIP was also abrogated in cells treated with DNA-damaging agents including UV, gamma-irradiation, and adriamycin, a response correlated with BRCA1 phosphorylation. Doxorubicin 133-143 BRCA1 DNA repair associated Homo sapiens 172-177 9679765-0 1998 Down-regulation of BRCA1 and BRCA2 in human ovarian cancer cells exposed to adriamycin and ultraviolet radiation. Doxorubicin 76-86 BRCA1 DNA repair associated Homo sapiens 19-24 9679765-4 1998 We found that Adriamycin (ADR) and ultraviolet (UV)radiation significantly down-regulated BRCA1 and BRCA2 mRNA expression in SK-OV-3 cells. Doxorubicin 14-24 BRCA1 DNA repair associated Homo sapiens 90-95 12170778-2 2002 We find that the Xeroderma Pigmentosum Complementation group E (XPE) mutated Damaged-DNA binding protein p48 (DDB2) is upregulated by BRCA1 in a p53-dependent manner following UVC, Adriamycin, or Cisplatin exposure. Doxorubicin 181-191 BRCA1 DNA repair associated Homo sapiens 134-139 10764811-9 2000 Finally, the interaction between CtIP and BRCA1 is shown to be stable in the face of genotoxic stress elicited by treatment with UV light, adriamycin, or hydrogen peroxide. Doxorubicin 139-149 BRCA1 DNA repair associated Homo sapiens 42-47 10344722-5 1999 RESULTS: Of 26 agents screened, BRCA1 and BRCA2 mRNA reductions were observed in both cell lines after exposure to adriamycin (ADR), camptothecin (CPT), sodium selenite (SLN), and ultraviolet radiation (UV), while nitrogen mustard (HN2) caused mRNA reduction in DU-145 but not in Tsu-Prl. Doxorubicin 115-125 BRCA1 DNA repair associated Homo sapiens 32-37 9619832-4 1998 We found that several agents, including adriamycin (a DNA intercalator and inhibitor of topoisomerase II), camptothecin (a topoisomerase I inhibitor), and ultraviolet radiation induced significant decreases in BRCA1 and BRCA2 mRNA levels. Doxorubicin 40-50 BRCA1 DNA repair associated Homo sapiens 210-215 9619832-5 1998 Decreased levels of BRCA1 and BRCA2 mRNAs were observed within 6-12 h after treatment with adriamycin and persisted for at least 72 h. Adriamycin also induced decreases in BRCA1 protein levels; but these decreases required several days. Doxorubicin 91-101 BRCA1 DNA repair associated Homo sapiens 20-25 9619832-5 1998 Decreased levels of BRCA1 and BRCA2 mRNAs were observed within 6-12 h after treatment with adriamycin and persisted for at least 72 h. Adriamycin also induced decreases in BRCA1 protein levels; but these decreases required several days. Doxorubicin 135-145 BRCA1 DNA repair associated Homo sapiens 20-25 9619832-5 1998 Decreased levels of BRCA1 and BRCA2 mRNAs were observed within 6-12 h after treatment with adriamycin and persisted for at least 72 h. Adriamycin also induced decreases in BRCA1 protein levels; but these decreases required several days. Doxorubicin 135-145 BRCA1 DNA repair associated Homo sapiens 172-177 9619832-8 1998 Adriamycin-induced down-regulation of BRCA1 and BRCA2 mRNAs was first observed at doses that yielded relatively little cytotoxicity and little or no apoptotic DNA fragmentation. Doxorubicin 0-10 BRCA1 DNA repair associated Homo sapiens 38-43 9619832-11 1998 However, the adriamycin-induced reduction in BRCA1 and BRCA2 mRNA levels was correlated with p53 functional status. Doxorubicin 13-23 BRCA1 DNA repair associated Homo sapiens 45-50 9619832-12 1998 MCF-7 cells transfected with a dominant negative mutant p53 (143 val-->ala) required at least tenfold higher doses of adriamycin to down-regulate BRCA1 and BRCA2 mRNAs than did parental MCF-7 cells or control-transfected MCF-7 clones. Doxorubicin 121-131 BRCA1 DNA repair associated Homo sapiens 149-154 35242827-3 2022 Methods: In a single-center cross-sectional study, stage I-III breast cancer survivors were enrolled according to three groups: (1) BRCA1/2 mutation carriers treated with doxorubicin; (2) BRCA1/2 mutation non-carriers treated with doxorubicin; and (3) BRCA1/2 mutation carriers treated with non-doxorubicin cancer therapy. Doxorubicin 171-182 BRCA1 DNA repair associated Homo sapiens 132-139 35242827-8 2022 In doxorubicin-treated BRCA1/2 mutation carriers and non-carriers, LVEF was lower by 5.4% (95% CI; -9.3, -1.5) and 4.8% (95% CI; -9.1, -0.5), respectively compared to carriers without doxorubicin exposure. Doxorubicin 3-14 BRCA1 DNA repair associated Homo sapiens 23-30 35242827-8 2022 In doxorubicin-treated BRCA1/2 mutation carriers and non-carriers, LVEF was lower by 5.4% (95% CI; -9.3, -1.5) and 4.8% (95% CI; -9.1, -0.5), respectively compared to carriers without doxorubicin exposure. Doxorubicin 184-195 BRCA1 DNA repair associated Homo sapiens 23-30 33536037-0 2021 Neoadjuvant therapy of BRCA1-driven ovarian cancer by combination of cisplatin, mitomycin C and doxorubicin. Doxorubicin 96-107 BRCA1 DNA repair associated Homo sapiens 23-28 33896588-14 2021 A multivariable analysis showed that harboring a germline BRCA mutation was related to a higher incidence of HSRs (HR: 1.84, 95% CI 1.00-3.99, p = 0.05) while having received pegylated liposomal doxorubicin (PLD) was related to a lower incidence of HSRs (HR: 0.03 95% CI 0.004-0.22, p = 0.001). Doxorubicin 195-206 BRCA1 DNA repair associated Homo sapiens 58-62 32876438-5 2020 Using this strategy, DOX-mediated cytotoxicity in Fanconi anemia group gene (FANC)/breast cancer susceptibility gene (BRCA)-deficient cells increased up to 70-fold compared to that in cells proficient in DNA repair pathways by increasing intracellular formaldehyde (FA) concentration. Doxorubicin 21-24 BRCA1 DNA repair associated Homo sapiens 118-122 33074587-8 2020 More importantly, suppressing BRCA1 expression in nasopharyngeal epithelial cell lines using miR-BART17-5p and miR-BART19-3p mimics reduced the DNA repair capability and increased the cell sensitivity to the DNA-damaging chemotherapeutic drugs, cisplatin and doxorubicin. Doxorubicin 259-270 BRCA1 DNA repair associated Homo sapiens 30-35 32876438-8 2020 Overall, anticancer therapy targeting tumors deficient in the FANC/BRCA pathway may be possible by minimizing DOX-induced toxicity in normal cells. Doxorubicin 110-113 BRCA1 DNA repair associated Homo sapiens 67-71 31411802-8 2019 BRCA1/2 mutations were significantly associated with age; personal and family history; FIGO stage; secondary recurrence interval; sensitivity to platinum in 1st, 2nd and 3rd line treatment; and response to doxorubicin liposomes. Doxorubicin 206-217 BRCA1 DNA repair associated Homo sapiens 0-7 32331767-10 2020 These findings were mechanistically confirmed in an in vitro mouse oocyte BRCA knockdown bioassay, which showed that BRCA deficiency results in increased oocyte susceptibility to doxorubicin. Doxorubicin 179-190 BRCA1 DNA repair associated Homo sapiens 74-78 31511498-1 2019 Adriamycin(ADR) is still considered to be one of the most effective agents in the treatment of breast cancer (BrCa), its efficacy is compromised by intrinsic resistance or acquire characteristics of multidrug resistance. Doxorubicin 0-10 BRCA1 DNA repair associated Homo sapiens 110-114 29784019-8 2018 CONCLUSIONS: This study suggests that combined use of a PARP inhibitor with doxorubicin, a DNA damaging agent, might be effective in the treatment of osteosarcoma patients, especially in the poor-prognostic subgroups of osteosarcoma expressing PARP1, gammaH2AX, or BRCA1/2. Doxorubicin 76-87 BRCA1 DNA repair associated Homo sapiens 265-272 30028120-2 2018 Owing to the ability of let-7a to repress DNA repair mechanisms (e.g., BRCA1 and BRCA2) and downregulate drug efflux pumps (e.g., ABCG2), delivery of let-7a could sensitize chemoresistant breast cancer cells (MDA-MB-231) to subsequent doxorubicin chemotherapy both in vitro and in vivo. Doxorubicin 235-246 BRCA1 DNA repair associated Homo sapiens 71-76 31215481-9 2019 Furthermore, the expression of HR repair factors (Rad51 and BRCA1) induced by doxorubicin was detected by Western blot and immunofluorescent staining in H446AR cells transfected with miR-7-5p mimic. Doxorubicin 78-89 BRCA1 DNA repair associated Homo sapiens 60-65 31215481-12 2019 MiR-7-5p impeded Dox-induced HR repair by inhibiting the expression of HR repair factors (Rad51 and BRCA1) that resulted in resensitizing SCLC cells to doxorubicin. Doxorubicin 17-20 BRCA1 DNA repair associated Homo sapiens 100-105 31215481-12 2019 MiR-7-5p impeded Dox-induced HR repair by inhibiting the expression of HR repair factors (Rad51 and BRCA1) that resulted in resensitizing SCLC cells to doxorubicin. Doxorubicin 152-163 BRCA1 DNA repair associated Homo sapiens 100-105 29929045-10 2018 However, FANCD2, BRCA1 and XRCC1 foci, prominently associated with 53BP1 foci and hence DSBs resolved by cNHEJ, were only detected in doxorubicin-treated XRCC4-deficient cells. Doxorubicin 134-145 BRCA1 DNA repair associated Homo sapiens 17-22 27555886-2 2016 For example, tumors in BRCA1/2 mutation carriers usually arise via somatic inactivation of the remaining BRCA allele, which makes them particularly sensitive to platinum-based drugs, PARP inhibitors (PARPi), mitomycin C, liposomal doxorubicin, etc. Doxorubicin 231-242 BRCA1 DNA repair associated Homo sapiens 23-28 29686231-3 2018 Here, we report that tamoxifen-resistant breast cancer cells express significantly more BARD1 and BRCA1, leading to resistance to DNA-damaging chemotherapy including cisplatin and adriamycin, but not to paclitaxel. Doxorubicin 180-190 BRCA1 DNA repair associated Homo sapiens 98-103 29298688-0 2018 Enhanced response rate to pegylated liposomal doxorubicin in high grade serous ovarian carcinomas harbouring BRCA1 and BRCA2 aberrations. Doxorubicin 46-57 BRCA1 DNA repair associated Homo sapiens 109-114 28881292-7 2017 In cells with BRCA1 silenced down, expression of UBE2C was obviously increased, with a concurrent decrease in cellular sensitivity to doxorubicin. Doxorubicin 134-145 BRCA1 DNA repair associated Homo sapiens 14-19 28881292-11 2017 Moreover, loss of BRCA1 function results in an increase in UBE2C expression and chemical resistance to doxorubicin in breast cancer cells. Doxorubicin 103-114 BRCA1 DNA repair associated Homo sapiens 18-23 26785283-5 2016 These features of BMOC are attributed to homologous-recombination repair deficiency in the absence of BRCA1/2 function, which results in an impaired ability of tumor cells to repair platinum-induced double-strand breaks, thereby conferring increased chemosensitivity and increased sensitivity to poly(ADP-ribose) polymerase enzyme inhibition and other DNA-damaging chemotherapeutic agents such as pegylated liposomal doxorubicin (PLD). Doxorubicin 417-428 BRCA1 DNA repair associated Homo sapiens 102-109 27555886-2 2016 For example, tumors in BRCA1/2 mutation carriers usually arise via somatic inactivation of the remaining BRCA allele, which makes them particularly sensitive to platinum-based drugs, PARP inhibitors (PARPi), mitomycin C, liposomal doxorubicin, etc. Doxorubicin 231-242 BRCA1 DNA repair associated Homo sapiens 23-27 27113739-0 2016 Neo-adjuvant doxorubicin and cyclophosphamide followed by paclitaxel in triple-negative breast cancer among BRCA1 mutation carriers and non-carriers. Doxorubicin 13-24 BRCA1 DNA repair associated Homo sapiens 108-113 26027929-5 2015 We identify MERIT40, a component of the BRCA1-A DNA damage repair complex, as an Akt substrate that is phosphorylated following doxorubicin treatment. Doxorubicin 128-139 BRCA1 DNA repair associated Homo sapiens 40-45 26027929-6 2015 MERIT40 phosphorylation facilitates assembly of the BRCA1-A complex in response to DNA damage and contributes to DNA repair and cell survival following doxorubicin treatment. Doxorubicin 152-163 BRCA1 DNA repair associated Homo sapiens 52-57 25993149-2 2015 These features of BMOC are attributed to homologous-recombination repair (HR) deficiency in the absence of BRCA1/2 function, which results in an impaired ability of tumor cells to repair platinum-induced double-strand breaks (DSBs), thereby conferring increased chemosensitivity and increased sensitivity to poly(ADP-ribose) polymerase (PARP) enzyme inhibition and other DNA-damaging chemotherapeutic agents such as pegylated liposomal doxorubicin (PLD). Doxorubicin 436-447 BRCA1 DNA repair associated Homo sapiens 107-114 24996439-0 2015 The Fanconi anemia/BRCA pathway is involved in DNA interstrand cross-link repair of adriamycin-resistant leukemia cells. Doxorubicin 84-94 BRCA1 DNA repair associated Homo sapiens 19-23 24996439-2 2015 Here we demonstrate that the FA/BRCA pathway contributes to acquired drug resistance in adriamycin (ADR)-resistant leukemia cell lines, and disruption of this pathway partially reverses the drug resistance. Doxorubicin 88-98 BRCA1 DNA repair associated Homo sapiens 32-36 23376355-0 2013 3,3"-Diindolymethane ameliorates adriamycin-induced cardiac fibrosis via activation of a BRCA1-dependent anti-oxidant pathway. Doxorubicin 33-43 BRCA1 DNA repair associated Homo sapiens 89-94 25337234-0 2014 Effect of adriamycin on BRCA1 and PARP-1 expression in MCF-7 breast cancer cells. Doxorubicin 10-20 BRCA1 DNA repair associated Homo sapiens 24-29 25337234-1 2014 To study the effects of adriamycin on the expression of BRCA1 and PARP-1 in BRCA1 wild-type MCF-7 cells. Doxorubicin 24-34 BRCA1 DNA repair associated Homo sapiens 56-61 25337234-1 2014 To study the effects of adriamycin on the expression of BRCA1 and PARP-1 in BRCA1 wild-type MCF-7 cells. Doxorubicin 24-34 BRCA1 DNA repair associated Homo sapiens 76-81 25337234-2 2014 We used Western blotting to detect BRCA1 and PARP-1 levels in MCF-7 cells treated with adriamycin, and used flow cytometry to detect apoptotic MCF-7 cells. Doxorubicin 87-97 BRCA1 DNA repair associated Homo sapiens 35-40 25337234-4 2014 BRCA1 levels were also increased upon treatment with a high dose of adriamycin, but gradually decreased over time. Doxorubicin 68-78 BRCA1 DNA repair associated Homo sapiens 0-5 25337234-7 2014 Compared to BRCA1-defective HCC1937 cells, adriamycin combined with 3-ABA can further induce apoptosis of MCF-7 cells (P < 0.05). Doxorubicin 43-53 BRCA1 DNA repair associated Homo sapiens 12-17 25337234-8 2014 All of these suggested that adriamycin can affect the PARP-1 activation and the expression of BRCA1. Doxorubicin 28-38 BRCA1 DNA repair associated Homo sapiens 94-99 23670255-2 2013 Previously, we identified GADD153 as a target of BRCA1 protein, which increases doxorubicin sensitivity in human p53 -/- PCa cells (PC3). Doxorubicin 80-91 BRCA1 DNA repair associated Homo sapiens 49-54 23670255-4 2013 METHODS: We performed reverse transcription quantitative PCR (RT-qPCR), western blot and luciferase assays to analyze GADD153 and/or BRCA1 expression in response to ultraviolet or doxorubicin exposure in PC3 p53 stable-transfected cells and LNCaP (p53+/+) cells. Doxorubicin 180-191 BRCA1 DNA repair associated Homo sapiens 133-138 23548133-6 2013 Pegylated liposomal doxorubicin may be considered as a promising treatment option for BRCA1/2-related ovarian cancer after the failure of platinum-containing therapy. Doxorubicin 20-31 BRCA1 DNA repair associated Homo sapiens 86-91 21864706-0 2011 BRCA1 is required for hMLH1 stabilization following doxorubicin-induced DNA damage. Doxorubicin 52-63 BRCA1 DNA repair associated Homo sapiens 0-5 22807977-2 2012 Thus, we hypothesized that BRCA1 protein expression and activating PIK3CA mutations are potential tumor biomarkers for the chemotherapeutic response to doxorubicin/cyclophosphamide plus docetaxel in locally advanced breast cancer. Doxorubicin 152-163 BRCA1 DNA repair associated Homo sapiens 27-32 22832221-6 2012 We have demonstrated that BRCA1 binds to ATM promoter and after doxorubicin exposure, it is released. Doxorubicin 64-75 BRCA1 DNA repair associated Homo sapiens 26-31 22832221-15 2012 Doxorubicin exposure releases BRCA1 and CtIP from ATM promoter still keeping E2F1 recruited and, in turn, represses ATM expression. Doxorubicin 0-11 BRCA1 DNA repair associated Homo sapiens 30-35 21864706-2 2011 In this study, we show that the activation of the MMR component hMLH1 in response to doxorubicin (DOX) treatment requires the presence of BRCA1 and that this phenomenon is mediated by an ATM/ATR dependent phosphorylation of the hMLH1 Ser-406 residue. Doxorubicin 85-96 BRCA1 DNA repair associated Homo sapiens 138-143 21864706-2 2011 In this study, we show that the activation of the MMR component hMLH1 in response to doxorubicin (DOX) treatment requires the presence of BRCA1 and that this phenomenon is mediated by an ATM/ATR dependent phosphorylation of the hMLH1 Ser-406 residue. Doxorubicin 98-101 BRCA1 DNA repair associated Homo sapiens 138-143 21864706-5 2011 We found that: (i) the negative modulation of BRCA1 expression is able to produce a remarkable reversal of hMLH1 stabilization, (ii) BRCA1 is required for post-translational modification produced by DOX treatment on hMLH1 which is, in turn, attributed to the ATM/ATR activity, (iii) the serine 406 phosphorylatable residue is critical for hMLH1 activation by ATM/ATR via BRCA1. Doxorubicin 199-202 BRCA1 DNA repair associated Homo sapiens 46-51 21864706-5 2011 We found that: (i) the negative modulation of BRCA1 expression is able to produce a remarkable reversal of hMLH1 stabilization, (ii) BRCA1 is required for post-translational modification produced by DOX treatment on hMLH1 which is, in turn, attributed to the ATM/ATR activity, (iii) the serine 406 phosphorylatable residue is critical for hMLH1 activation by ATM/ATR via BRCA1. Doxorubicin 199-202 BRCA1 DNA repair associated Homo sapiens 133-138 21864706-5 2011 We found that: (i) the negative modulation of BRCA1 expression is able to produce a remarkable reversal of hMLH1 stabilization, (ii) BRCA1 is required for post-translational modification produced by DOX treatment on hMLH1 which is, in turn, attributed to the ATM/ATR activity, (iii) the serine 406 phosphorylatable residue is critical for hMLH1 activation by ATM/ATR via BRCA1. Doxorubicin 199-202 BRCA1 DNA repair associated Homo sapiens 133-138 21835933-0 2011 BRCA mutation status and determinant of outcome in women with recurrent epithelial ovarian cancer treated with pegylated liposomal doxorubicin. Doxorubicin 131-142 BRCA1 DNA repair associated Homo sapiens 0-4 21945552-0 2011 A high response rate to liposomal doxorubicin is seen among women with BRCA mutations treated for recurrent epithelial ovarian cancer. Doxorubicin 34-45 BRCA1 DNA repair associated Homo sapiens 71-75 19593673-6 2009 The molecular changes in both cell lines due to DOX treatment could be classified into: (1) the basal level of p53, p21, BRCA1, GST and TOPOIIalpha mRNA was higher in MCF7/DOX than MCF7/WT. Doxorubicin 48-51 BRCA1 DNA repair associated Homo sapiens 121-126 19820363-1 2009 BACKGROUND: The aim of the study was to assess the efficacy of pegylated liposomal doxorubicin (PLD) and oxaliplatin in patients affected by relapsed epithelial ovarian cancer with a family history of BRCA and p53 mutations. Doxorubicin 83-94 BRCA1 DNA repair associated Homo sapiens 201-205 21700680-0 2011 BRCA1 loss induces GADD153-mediated doxorubicin resistance in prostate cancer. Doxorubicin 36-47 BRCA1 DNA repair associated Homo sapiens 0-5 21700680-4 2011 BRCA1 expression mediates apoptosis, cell-cycle arrest, and decreased viability in response to doxorubicin treatment. Doxorubicin 95-106 BRCA1 DNA repair associated Homo sapiens 0-5 21700680-8 2011 Finally, GADD153 depletion significantly abrogates BRCA1 influence on cell-cycle progression and cell death in response to doxorubicin treatment. Doxorubicin 123-134 BRCA1 DNA repair associated Homo sapiens 51-56