PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34132814-18 2021 These findings suggest the variant allele C of T2285C polymorphism of PARP1 linked to an increase of NSCLC risk, and unfavorable efficacy and prognosis of NSCLC patients with platinum-based chemotherapy, which might be associated with enhancement of its mRNA expression and the diminishment of activity. Platinum 175-183 poly(ADP-ribose) polymerase 1 Homo sapiens 70-75 9380409-3 1997 Here we show that induction of PT is sufficient to activate CPP32-like proteases with DEVDase activity and the associated cleavage of the nuclear DEVDase substrate poly(ADP-ribose) polymerase (PARP). Platinum 31-33 poly(ADP-ribose) polymerase 1 Homo sapiens 193-197 24882434-1 2014 BACKGROUND: Maintenance monotherapy with the PARP inhibitor olaparib significantly prolonged progression-free survival (PFS) versus placebo in patients with platinum-sensitive recurrent serous ovarian cancer. Platinum 157-165 poly(ADP-ribose) polymerase 1 Homo sapiens 45-49 34520432-0 2021 PARP inhibitors decrease response to subsequent platinum-based chemotherapy in patients with BRCA mutated ovarian cancer. Platinum 48-56 poly(ADP-ribose) polymerase 1 Homo sapiens 0-4 34948122-9 2021 Since the BIN1 gene rarely mutates in human cancers, our results suggest that simultaneous inhibition of PARP1 and ATM provokes a new BRCAness-independent synthetic lethal effect and ultimately re-establishes cisplatin sensitivity even in platinum-refractory cancer cells. Platinum 239-247 poly(ADP-ribose) polymerase 1 Homo sapiens 105-110 34955157-3 2021 Treatments with PARP inhibitors is a major advance in medical management with significant efficacy in maintenance after response to platinum-based chemotherapy. Platinum 132-140 poly(ADP-ribose) polymerase 1 Homo sapiens 16-20 34900739-0 2021 Comparison of the Efficacy and Safety of PARP Inhibitors as a Monotherapy for Platinum-Sensitive Recurrent Ovarian Cancer: A Network Meta-Analysis. Platinum 78-86 poly(ADP-ribose) polymerase 1 Homo sapiens 41-45 34593416-5 2021 However, not only PARP inhibitors, but also chemotherapeutic agents such as platinum agents, taxanes, and radium-223 are active in HRR gene mutation carriers, and platinum sensitivity may predict the efficacy of PARP inhibitors for mCRPC. Platinum 163-171 poly(ADP-ribose) polymerase 1 Homo sapiens 18-22 34593416-5 2021 However, not only PARP inhibitors, but also chemotherapeutic agents such as platinum agents, taxanes, and radium-223 are active in HRR gene mutation carriers, and platinum sensitivity may predict the efficacy of PARP inhibitors for mCRPC. Platinum 163-171 poly(ADP-ribose) polymerase 1 Homo sapiens 212-216 34616492-1 2021 Background: In patients with newly diagnosed ovarian cancer, bevacizumab and poly(ADP-ribose) polymerase (PARP) inhibitors, alone or in combination, have shown benefit as maintenance treatment following platinum-based chemotherapy. Platinum 203-211 poly(ADP-ribose) polymerase 1 Homo sapiens 77-104 34616492-1 2021 Background: In patients with newly diagnosed ovarian cancer, bevacizumab and poly(ADP-ribose) polymerase (PARP) inhibitors, alone or in combination, have shown benefit as maintenance treatment following platinum-based chemotherapy. Platinum 203-211 poly(ADP-ribose) polymerase 1 Homo sapiens 106-110 35219776-1 2022 BACKGROUND: Maintenance treatment with poly (ADP-ribose) polymerase (PARP) inhibitor is now the standard of care in patients with BRCA mutated platinum-sensitive recurrent ovarian cancer following response to chemotherapy. Platinum 143-151 poly(ADP-ribose) polymerase 1 Homo sapiens 39-67 35219776-1 2022 BACKGROUND: Maintenance treatment with poly (ADP-ribose) polymerase (PARP) inhibitor is now the standard of care in patients with BRCA mutated platinum-sensitive recurrent ovarian cancer following response to chemotherapy. Platinum 143-151 poly(ADP-ribose) polymerase 1 Homo sapiens 69-73 35396812-1 2022 BACKGROUND: Inhibitors of poly(ADP-ribose) polymerase (PARP) proteins potentiate antitumor activity of platinum chemotherapy. Platinum 103-111 poly(ADP-ribose) polymerase 1 Homo sapiens 26-53 35396812-1 2022 BACKGROUND: Inhibitors of poly(ADP-ribose) polymerase (PARP) proteins potentiate antitumor activity of platinum chemotherapy. Platinum 103-111 poly(ADP-ribose) polymerase 1 Homo sapiens 55-59 33515422-3 2021 However, there is no doubt that the incorporation of PARP inhibitors as maintenance after the response to platinum-based chemotherapy, first in recurrent disease and recently also in first line, will change the natural history of the disease.The objective of this guide is to summarize the current evidence for the diagnosis, treatment, and follow-up of ovarian cancer, and to provide evidence-based recommendations for clinical practice. Platinum 106-114 poly(ADP-ribose) polymerase 1 Homo sapiens 53-57 35124372-3 2022 Poly(ADP-Ribose) polymerase 1 (PARP1) is an enzyme crucial for repairing DNA damage induced by platinum compounds, which undermines the effectiveness of platinum-based chemotherapy. Platinum 95-103 poly(ADP-ribose) polymerase 1 Homo sapiens 0-29 35124372-3 2022 Poly(ADP-Ribose) polymerase 1 (PARP1) is an enzyme crucial for repairing DNA damage induced by platinum compounds, which undermines the effectiveness of platinum-based chemotherapy. Platinum 95-103 poly(ADP-ribose) polymerase 1 Homo sapiens 31-36 35124372-3 2022 Poly(ADP-Ribose) polymerase 1 (PARP1) is an enzyme crucial for repairing DNA damage induced by platinum compounds, which undermines the effectiveness of platinum-based chemotherapy. Platinum 153-161 poly(ADP-ribose) polymerase 1 Homo sapiens 0-29 35124372-3 2022 Poly(ADP-Ribose) polymerase 1 (PARP1) is an enzyme crucial for repairing DNA damage induced by platinum compounds, which undermines the effectiveness of platinum-based chemotherapy. Platinum 153-161 poly(ADP-ribose) polymerase 1 Homo sapiens 31-36 35124372-9 2022 Our finding that the TOPBP1/PARP1 pathway facilitates acquisition of oxaliplatin resistance uncovers a novel mechanism underlying platinum-based chemotherapy resistance in gastric cancer that may be utilized for developing effective therapeutic strategies. Platinum 130-138 poly(ADP-ribose) polymerase 1 Homo sapiens 28-33 35018214-2 2022 However, platinum-based chemopotentiation by PARP inhibitors (PARPi), particularly for non-small cell lung cancer (NSCLC), has only been confirmed in a few preclinical models and the molecular mechanisms that drive PARPi combinatorial synergy with chemotherapeutics remains poorly defined. Platinum 9-17 poly(ADP-ribose) polymerase 1 Homo sapiens 45-49 33675937-6 2021 For patients with recurrent high grade ovarian cancer, which responds to platinum-based treatment maintenance therapy with a poly(ADP-ribose) polymerase (PARP) inhibitor can be offered, regardless of BRCA mutation status. Platinum 73-81 poly(ADP-ribose) polymerase 1 Homo sapiens 125-152 33675937-6 2021 For patients with recurrent high grade ovarian cancer, which responds to platinum-based treatment maintenance therapy with a poly(ADP-ribose) polymerase (PARP) inhibitor can be offered, regardless of BRCA mutation status. Platinum 73-81 poly(ADP-ribose) polymerase 1 Homo sapiens 154-158 33743851-1 2021 BACKGROUND: Olaparib, a poly (ADP-ribose) polymerase (PARP) inhibitor, has previously been shown to extend progression-free survival versus placebo when given to patients with relapsed high-grade serous or endometrioid ovarian cancer who were platinum sensitive and who had a BRCA1 or BRCA2 (BRCA1/2) mutation, as part of the SOLO2/ENGOT-Ov21 trial. Platinum 243-251 poly(ADP-ribose) polymerase 1 Homo sapiens 54-58 33882241-5 2021 Several PARP inhibitors, which target defective DNA repair have been approved as maintenance therapy for advanced ovarian cancer in both the first line and platinum sensitive relapsed settings. Platinum 156-164 poly(ADP-ribose) polymerase 1 Homo sapiens 8-12 33926263-0 2022 Effect of PARP Inhibitors as Maintenance Treatment on Restricted Mean Survival Time in Platinum-Sensitive Recurrent Ovarian Cancer: A Systematic Review and Meta-analysis. Platinum 87-95 poly(ADP-ribose) polymerase 1 Homo sapiens 10-14 33926263-1 2022 BACKGROUND: Earlier trials on the efficacy of poly (ADP-ribose) polymerase (PARP) inhibitors in platinum-sensitive relapsed ovarian cancer used the hazard ratio (HR) as an efficacy parameter. Platinum 96-104 poly(ADP-ribose) polymerase 1 Homo sapiens 46-74 33926263-1 2022 BACKGROUND: Earlier trials on the efficacy of poly (ADP-ribose) polymerase (PARP) inhibitors in platinum-sensitive relapsed ovarian cancer used the hazard ratio (HR) as an efficacy parameter. Platinum 96-104 poly(ADP-ribose) polymerase 1 Homo sapiens 76-80 33920140-1 2021 Poly (ADP-ribose) polymerase 1 inhibitors (PARPi) are used to treat recurrent ovarian cancer (OC) patients due to greater survival benefits and minimal side effects, especially in those patients with complete or partial response to platinum-based chemotherapy. Platinum 232-240 poly(ADP-ribose) polymerase 1 Homo sapiens 0-30 33617901-4 2021 The FDA and EMA has recently approved olaparib, a Poly (ADP-ribose) polymerase (PARP) inhibitor, as a maintenance strategy for platinum-sensitive advanced PDAC patients with BRCA mutations. Platinum 127-135 poly(ADP-ribose) polymerase 1 Homo sapiens 80-84 33423551-2 2021 Despite novel compound classes like vascular endothelial growth factor (VEGF) inhibitors or poly-ADP ribose polymerase (PARP) inhibitors are available, which improve significantly efficacy of platinum-based chemotherapy, OC prognosis remains poor and innovative strategies are needed. Platinum 192-200 poly(ADP-ribose) polymerase 1 Homo sapiens 92-118 33724122-7 2021 In this way, PARP inhibitors can obtain an important role in making a personalized therapeutic program in case of first-line, neoadjuvant, platinum-sensitive and resistant high-grade serous OC treatment. Platinum 139-147 poly(ADP-ribose) polymerase 1 Homo sapiens 13-17 33740262-0 2021 Molecular and clinical predictors of improvement in progression-free survival with maintenance PARP inhibitor therapy in women with platinum-sensitive, recurrent ovarian cancer: A meta-analysis. Platinum 132-140 poly(ADP-ribose) polymerase 1 Homo sapiens 95-99 33692936-0 2020 Comparative Efficacy and Safety of PARP Inhibitors as Maintenance Therapy in Platinum Sensitive Recurrent Ovarian Cancer: A Network Meta-Analysis. Platinum 77-85 poly(ADP-ribose) polymerase 1 Homo sapiens 35-39 33669671-5 2021 However, and in contrast with the findings of others, we detected no synergistic effect between olaparib and oxaliplatin, and we found that the Akt pathway inhibitor augmented the cytostatic properties of the platinum compound and/or prevented the cytoprotective effects of PARP inhibition. Platinum 209-217 poly(ADP-ribose) polymerase 1 Homo sapiens 274-278 33423551-2 2021 Despite novel compound classes like vascular endothelial growth factor (VEGF) inhibitors or poly-ADP ribose polymerase (PARP) inhibitors are available, which improve significantly efficacy of platinum-based chemotherapy, OC prognosis remains poor and innovative strategies are needed. Platinum 192-200 poly(ADP-ribose) polymerase 1 Homo sapiens 120-124 33478135-2 2021 The objective of our study was to evaluate the expression of an important DNA repair enzyme, the Poly (ADP-Ribose) Polymerase (PARP) expression in epithelial ovarian cancer (EOC) tissues depending on BRCA status and to assess its relationship with platinum resistance. Platinum 248-256 poly(ADP-ribose) polymerase 1 Homo sapiens 97-125 33478135-2 2021 The objective of our study was to evaluate the expression of an important DNA repair enzyme, the Poly (ADP-Ribose) Polymerase (PARP) expression in epithelial ovarian cancer (EOC) tissues depending on BRCA status and to assess its relationship with platinum resistance. Platinum 248-256 poly(ADP-ribose) polymerase 1 Homo sapiens 127-131 33250205-1 2021 PURPOSE: Maintenance therapy with the poly(ADP-ribose) polymerase (PARP) inhibitor olaparib provided a substantial progression-free survival (PFS) benefit compared with placebo in patients with newly diagnosed advanced ovarian cancer and a BRCA mutation (BRCAm) who were in clinical complete or partial response following platinum-based chemotherapy in the Phase III SOLO1 global study. Platinum 322-330 poly(ADP-ribose) polymerase 1 Homo sapiens 67-71 33068886-1 2020 Poly ADP -Ribose Polymerase (PARP) inhibitors (PARPi) were firstly licensed for maintenance treatment in recurrent, platinum-sensitive, platinum responsive epithelial ovarian cancer patients, harboring or not a BRCA mutation. Platinum 116-124 poly(ADP-ribose) polymerase 1 Homo sapiens 0-27 33068886-1 2020 Poly ADP -Ribose Polymerase (PARP) inhibitors (PARPi) were firstly licensed for maintenance treatment in recurrent, platinum-sensitive, platinum responsive epithelial ovarian cancer patients, harboring or not a BRCA mutation. Platinum 116-124 poly(ADP-ribose) polymerase 1 Homo sapiens 29-33 33068886-1 2020 Poly ADP -Ribose Polymerase (PARP) inhibitors (PARPi) were firstly licensed for maintenance treatment in recurrent, platinum-sensitive, platinum responsive epithelial ovarian cancer patients, harboring or not a BRCA mutation. Platinum 136-144 poly(ADP-ribose) polymerase 1 Homo sapiens 0-27 33068886-1 2020 Poly ADP -Ribose Polymerase (PARP) inhibitors (PARPi) were firstly licensed for maintenance treatment in recurrent, platinum-sensitive, platinum responsive epithelial ovarian cancer patients, harboring or not a BRCA mutation. Platinum 136-144 poly(ADP-ribose) polymerase 1 Homo sapiens 29-33 33147530-0 2020 A functional polymorphism in the poly(ADP-ribose) polymerase-1 gene is associated with platinum-based chemotherapeutic response and prognosis in epithelial ovarian cancer patients. Platinum 87-95 poly(ADP-ribose) polymerase 1 Homo sapiens 33-62 33147530-1 2020 OBJECTIVE: To explore the effects of two functional genetic variants of poly(ADP-ribose) polymerase-1 (PARP-1) on the susceptibility to epithelial ovarian cancer (EOC), the platinum-based chemotherapeutic response, and the prognosis of northern Chinese patients. Platinum 173-181 poly(ADP-ribose) polymerase 1 Homo sapiens 72-101 33147530-1 2020 OBJECTIVE: To explore the effects of two functional genetic variants of poly(ADP-ribose) polymerase-1 (PARP-1) on the susceptibility to epithelial ovarian cancer (EOC), the platinum-based chemotherapeutic response, and the prognosis of northern Chinese patients. Platinum 173-181 poly(ADP-ribose) polymerase 1 Homo sapiens 103-109 32512040-5 2020 Recently, functional evidence from patient-derived xenografts and organoids have suggested that maintenance with PARP-inhibitors might represent a therapeutic opportunity in CRC patients previously responsive to platinum-based treatment. Platinum 212-220 poly(ADP-ribose) polymerase 1 Homo sapiens 113-117 32172572-8 2020 CONCLUSIONS: PARP inhibitors can be used as a single agent for maintenance therapy for platinum-sensitive recurrent disease in patients with partial or complete response following 2 or more rounds of platinum-based therapy. Platinum 87-95 poly(ADP-ribose) polymerase 1 Homo sapiens 13-17 32172572-8 2020 CONCLUSIONS: PARP inhibitors can be used as a single agent for maintenance therapy for platinum-sensitive recurrent disease in patients with partial or complete response following 2 or more rounds of platinum-based therapy. Platinum 200-208 poly(ADP-ribose) polymerase 1 Homo sapiens 13-17 32817083-1 2020 INTRODUCTION: We aimed to evaluate poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi) regimens in BRCA-mutated ovarian cancer for patients responsive to front-line platinum (bevacizumab and olaparib, veliparib and chemotherapy, olaparib) or platinum-sensitive relapsed (olaparib, rucaprib, niraparib) patients in phase III randomized controlled trials. Platinum 167-175 poly(ADP-ribose) polymerase 1 Homo sapiens 35-63 32817083-1 2020 INTRODUCTION: We aimed to evaluate poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi) regimens in BRCA-mutated ovarian cancer for patients responsive to front-line platinum (bevacizumab and olaparib, veliparib and chemotherapy, olaparib) or platinum-sensitive relapsed (olaparib, rucaprib, niraparib) patients in phase III randomized controlled trials. Platinum 167-175 poly(ADP-ribose) polymerase 1 Homo sapiens 65-69 32817083-1 2020 INTRODUCTION: We aimed to evaluate poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi) regimens in BRCA-mutated ovarian cancer for patients responsive to front-line platinum (bevacizumab and olaparib, veliparib and chemotherapy, olaparib) or platinum-sensitive relapsed (olaparib, rucaprib, niraparib) patients in phase III randomized controlled trials. Platinum 244-252 poly(ADP-ribose) polymerase 1 Homo sapiens 35-63 32817083-1 2020 INTRODUCTION: We aimed to evaluate poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi) regimens in BRCA-mutated ovarian cancer for patients responsive to front-line platinum (bevacizumab and olaparib, veliparib and chemotherapy, olaparib) or platinum-sensitive relapsed (olaparib, rucaprib, niraparib) patients in phase III randomized controlled trials. Platinum 244-252 poly(ADP-ribose) polymerase 1 Homo sapiens 65-69 33112397-1 2020 Importance: DNA repair gene aberrations occur in 20% to 30% of patients with castration-resistant prostate cancer (CRPC), and some of these aberrations have been associated with sensitivity to poly(ADP-ribose) polymerase (PARP) inhibition platinum-based treatments. Platinum 239-247 poly(ADP-ribose) polymerase 1 Homo sapiens 193-220 33112397-1 2020 Importance: DNA repair gene aberrations occur in 20% to 30% of patients with castration-resistant prostate cancer (CRPC), and some of these aberrations have been associated with sensitivity to poly(ADP-ribose) polymerase (PARP) inhibition platinum-based treatments. Platinum 239-247 poly(ADP-ribose) polymerase 1 Homo sapiens 222-226 32594311-13 2020 The lack of PARP expression assessed by immunohistochemistry may predict improved PFS in ovarian cancer patients after adjuvant platinum-based chemotherapy. Platinum 128-136 poly(ADP-ribose) polymerase 1 Homo sapiens 12-16 32569725-1 2020 BACKGROUND: In recurrent ovarian cancer, poly(ADP-ribose) polymerase (PARP)-inhibiting agents have transformed the treatment of platinum-sensitive disease. Platinum 128-136 poly(ADP-ribose) polymerase 1 Homo sapiens 41-68 32569725-1 2020 BACKGROUND: In recurrent ovarian cancer, poly(ADP-ribose) polymerase (PARP)-inhibiting agents have transformed the treatment of platinum-sensitive disease. Platinum 128-136 poly(ADP-ribose) polymerase 1 Homo sapiens 70-74 32981695-1 2020 OBJECTIVE: Niraparib is a poly(ADP-ribose) polymerase (PARP) inhibitor approved for use in heavily pretreated patients and as maintenance treatment in patients with newly-diagnosed or recurrent ovarian cancer following a response to platinum-based chemotherapy. Platinum 233-241 poly(ADP-ribose) polymerase 1 Homo sapiens 55-59 32878963-1 2020 BACKGROUND: With the success of poly(ADP-ribose) polymerase (PARP) inhibitor therapy in the first-line and second-line treatment settings, a new patient population is emerging with platinum-sensitive relapsed ovarian cancer, who have previously received a PARP inhibitor in the maintenance setting and for whom no second maintenance standard of care exists. Platinum 181-189 poly(ADP-ribose) polymerase 1 Homo sapiens 32-59 32878963-1 2020 BACKGROUND: With the success of poly(ADP-ribose) polymerase (PARP) inhibitor therapy in the first-line and second-line treatment settings, a new patient population is emerging with platinum-sensitive relapsed ovarian cancer, who have previously received a PARP inhibitor in the maintenance setting and for whom no second maintenance standard of care exists. Platinum 181-189 poly(ADP-ribose) polymerase 1 Homo sapiens 61-65 32878963-1 2020 BACKGROUND: With the success of poly(ADP-ribose) polymerase (PARP) inhibitor therapy in the first-line and second-line treatment settings, a new patient population is emerging with platinum-sensitive relapsed ovarian cancer, who have previously received a PARP inhibitor in the maintenance setting and for whom no second maintenance standard of care exists. Platinum 181-189 poly(ADP-ribose) polymerase 1 Homo sapiens 256-260 32321768-0 2020 Real world outcomes in platinum sensitive relapsed ovarian, fallopian tube, or peritoneal cancer treated in routine clinical practice in the United Kingdom prior to poly-ADP ribose polymerase inhibitors. Platinum 23-31 poly(ADP-ribose) polymerase 1 Homo sapiens 165-191 33006584-3 2020 PARP inhibitors are also approved as maintenance treatment following a response to platinum-based therapy in the recurrent setting, irrespective of biomarker status. Platinum 83-91 poly(ADP-ribose) polymerase 1 Homo sapiens 0-4 33006584-4 2020 Additionally, PARP inhibitors are approved as third-line treatment and beyond in lieu of chemotherapy for patients with BRCA-associated cancers, and as fourth-line treatment and beyond for patients with platinum-sensitive homologous recombination-deficient tumors. Platinum 203-211 poly(ADP-ribose) polymerase 1 Homo sapiens 14-18 32793315-1 2020 Background: Patients with DNA-damage response genes (DDR)-related pancreas cancer (BRCA1/2 or other DNA-damage related genes) may have improved outcomes secondary to increased sensitivity to DNA-damaging drugs (platinum chemotherapy/ poly ADP ribose polymerase (PARP)-inhibitors). Platinum 211-219 poly(ADP-ribose) polymerase 1 Homo sapiens 262-266 32953627-9 2020 More recently, the approach to secondary, tertiary, and later recurrence has been changed by the introduction of PARP inhibitors, which resulted effective as maintenance monotherapy in both platinum-sensitive and platinum-resistant recurrence when the genetic background of the tumor allows their application with a significant improvement of oncological outcomes. Platinum 190-198 poly(ADP-ribose) polymerase 1 Homo sapiens 113-117 32953627-9 2020 More recently, the approach to secondary, tertiary, and later recurrence has been changed by the introduction of PARP inhibitors, which resulted effective as maintenance monotherapy in both platinum-sensitive and platinum-resistant recurrence when the genetic background of the tumor allows their application with a significant improvement of oncological outcomes. Platinum 213-221 poly(ADP-ribose) polymerase 1 Homo sapiens 113-117 32321768-1 2020 INTRODUCTION: The introduction of poly-ADP ribose polymerase inhibitors in ovarian cancer has demonstrated significantly improved progression free survival in four randomized controlled clinical trials in patients with platinum sensitive relapsed ovarian cancer. Platinum 219-227 poly(ADP-ribose) polymerase 1 Homo sapiens 34-60 32601814-7 2020 How to move forward the preclinical promise of these newer DDR-targeting therapies into rational clinical trial combinations and sequence PARP inhibitors in relation to platinum chemotherapy remain areas of tremendous clinical research interest. Platinum 169-177 poly(ADP-ribose) polymerase 1 Homo sapiens 138-142 32575908-2 2020 In terms of maintenance therapies after platinum-based chemotherapy, PARP inhibitors significantly improve the overall survival of patients with BRCA mutations but is of little benefit to patients without homologous recombination deficiency (HRD). Platinum 40-48 poly(ADP-ribose) polymerase 1 Homo sapiens 69-73 32612955-15 2020 BRCA mutation, HRD-positive status, and sensitivity to platinum are effective prognostic factors for the efficacy of PARP inhibitors. Platinum 55-63 poly(ADP-ribose) polymerase 1 Homo sapiens 117-121 32471249-2 2020 In this setting, PARP inhibitors, either as single agent or in combination with platinum-based chemotherapy, significantly increased progression-free survival, as compared to conventional chemotherapy. Platinum 80-88 poly(ADP-ribose) polymerase 1 Homo sapiens 17-21 32471250-0 2020 Bevacizumab or PARP-Inhibitors Maintenance Therapy for Platinum-Sensitive Recurrent Ovarian Cancer: A Network Meta-Analysis. Platinum 55-63 poly(ADP-ribose) polymerase 1 Homo sapiens 15-19 32171277-8 2020 CONCLUSIONS: Here we report a case of a patient with prostate cancer who received a platinum agent and PARP inhibitor sequentially and in whom polyclonal BRCA2 reversion mutations were identified as the likely mechanism of acquired resistance to carboplatin and primary resistance to PARP inhibition. Platinum 84-92 poly(ADP-ribose) polymerase 1 Homo sapiens 284-288 32609666-6 2020 On the basis of the principle of synthetic lethality, and to avert resistance to PARP inhibitors, clinical trials of combination therapy with PARP inhibitors and platinum-based chemotherapy have been conducted with an early signal. Platinum 162-170 poly(ADP-ribose) polymerase 1 Homo sapiens 81-85 31074636-2 2019 Three different poly ADP ribose polymerase inhibitors (olaparib, niraparib and rucaparib) have been already approved as maintenance after response to platinum-based chemotherapy; two of them (olaparib and rucaparib) also as single agents. Platinum 150-158 poly(ADP-ribose) polymerase 1 Homo sapiens 16-42 31863638-4 2020 Olaparib is a PARP inhibitor approved for maintenance therapy following platinum-based chemotherapy. Platinum 72-80 poly(ADP-ribose) polymerase 1 Homo sapiens 14-18 31650446-7 2020 This "PARP trapping" potentiates synergism between PARP inhibition and both alkylating agents and platinum-based chemotherapy. Platinum 98-106 poly(ADP-ribose) polymerase 1 Homo sapiens 6-10 31902551-1 2020 OBJECTIVE: To evaluate the correlation between expression of p53, Livin, Excision repair cross-complementation group 1 (ERCC1), BRCA1 and Poly (ADP-ribose) polymerase 1 (PARP 1) in epithelial ovarian cancer (EOC) tissues with platinum-based chemotherapy and prognosis in patients who received either comprehensive surgical staging or cytoreductive surgery. Platinum 226-234 poly(ADP-ribose) polymerase 1 Homo sapiens 170-176 31856090-2 2020 Increasingly, the recommended treatment for those with a germline mutation in a gene involved in homologous recombination repair is with a platinum drug followed by a poly (ADP-ribose) polymerase (poly adenosine phosphate-ribose polymerase [PARP]) inhibitor. Platinum 139-147 poly(ADP-ribose) polymerase 1 Homo sapiens 241-245 31562799-1 2019 BACKGROUND: Niraparib, an inhibitor of poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP), has been associated with significantly increased progression-free survival among patients with recurrent ovarian cancer after platinum-based chemotherapy, regardless of the presence or absence of BRCA mutations. Platinum 225-233 poly(ADP-ribose) polymerase 1 Homo sapiens 92-96 31738050-3 2019 Both the synthesized PARPi ligands and PARPi-Pt conjugates [PARPi-Pt(IV)] show inhibitory effects against PARP-1"s catalytic activity. Platinum 45-47 poly(ADP-ribose) polymerase 1 Homo sapiens 106-112 31738050-3 2019 Both the synthesized PARPi ligands and PARPi-Pt conjugates [PARPi-Pt(IV)] show inhibitory effects against PARP-1"s catalytic activity. Platinum 66-72 poly(ADP-ribose) polymerase 1 Homo sapiens 106-112 31738050-6 2019 Our study provides a strategy to improve the cytotoxicity of platinum(IV)-based anticancer complexes and overcome cisplatin resistance by using a small-molecule anticancer complex that simultaneously damages DNA and inhibits PARP. Platinum 61-69 poly(ADP-ribose) polymerase 1 Homo sapiens 225-229 31478762-1 2019 The poly ADP ribose polymerase olaparib is currently approved in front line BRCA-associated epithelial ovarian cancer (EOC), platinum-sensitive recurrence agnostic to BRCA status and for gBRCA as treatment in the fourth line and beyond. Platinum 125-133 poly(ADP-ribose) polymerase 1 Homo sapiens 4-30 30895466-3 2019 Early clinical data demonstrated the effectiveness of PARP inhibition in women with recurrent EOC harbouring BRCA1/2 mutations and those with platinum-sensitive recurrences. Platinum 142-150 poly(ADP-ribose) polymerase 1 Homo sapiens 54-58 30895466-5 2019 Based upon randomised controlled trials, PARP inhibitors are in use as "maintenance" therapy for those with platinum-sensitive and platinum-responsive recurrences (irrespective of BRCA1/2 mutation status). Platinum 108-116 poly(ADP-ribose) polymerase 1 Homo sapiens 41-45 30895466-5 2019 Based upon randomised controlled trials, PARP inhibitors are in use as "maintenance" therapy for those with platinum-sensitive and platinum-responsive recurrences (irrespective of BRCA1/2 mutation status). Platinum 131-139 poly(ADP-ribose) polymerase 1 Homo sapiens 41-45 32186787-6 2020 Recently, phase 3 studies have shown that ovarian cancer patients with recurrent, platinum sensitive disease who were treated with PARP inhibitors have shown statistically significant improvement in progression free survival. Platinum 82-90 poly(ADP-ribose) polymerase 1 Homo sapiens 131-135 32186787-9 2020 Following these studies, the FDA and the European authorities granted an accelerated approval for the use of PARP inhibitors as maintenance treatment after first line treatment, for BRCA carriers, and at the recurrence for platinum sensitive patients. Platinum 223-231 poly(ADP-ribose) polymerase 1 Homo sapiens 109-113 31669203-1 2020 PARP1 inhibitor (Niraparib, Olaparib, Rucaparib) maintenance therapy improves progression-free survival in platinum sensitive sporadic epithelial ovarian cancers. Platinum 107-115 poly(ADP-ribose) polymerase 1 Homo sapiens 0-5 31721706-6 2020 Pt(II)-Bpy induced DNA damage, which was demonstrated through a marked increase in the expression of cleaved-poly (ADP ribose) polymerase (PARP) and gamma-H2A histone family member X and a decrease in PARP expression. Platinum 0-10 poly(ADP-ribose) polymerase 1 Homo sapiens 109-137 31721706-6 2020 Pt(II)-Bpy induced DNA damage, which was demonstrated through a marked increase in the expression of cleaved-poly (ADP ribose) polymerase (PARP) and gamma-H2A histone family member X and a decrease in PARP expression. Platinum 0-10 poly(ADP-ribose) polymerase 1 Homo sapiens 139-143 31721706-6 2020 Pt(II)-Bpy induced DNA damage, which was demonstrated through a marked increase in the expression of cleaved-poly (ADP ribose) polymerase (PARP) and gamma-H2A histone family member X and a decrease in PARP expression. Platinum 0-10 poly(ADP-ribose) polymerase 1 Homo sapiens 201-205 31553293-13 2020 Understanding the mechanism of resistance to PARP inhibitors and their relationship with platinum resistance may help with the development of antiresistance therapies and optimization of the sequence of drug application in the future clinical treatment of ovarian cancer. Platinum 89-97 poly(ADP-ribose) polymerase 1 Homo sapiens 45-49 31534014-1 2020 Poly (ADP-ribose) Polymerase (PARP) inhibitors (PARPi) are approved to treat recurrent ovarian cancer with BRCA1 or BRCA2 mutations, and as maintenance therapy for recurrent platinum sensitive ovarian cancer (BRCA wild-type or mutated) after treatment with platinum. Platinum 174-182 poly(ADP-ribose) polymerase 1 Homo sapiens 0-28 31534014-1 2020 Poly (ADP-ribose) Polymerase (PARP) inhibitors (PARPi) are approved to treat recurrent ovarian cancer with BRCA1 or BRCA2 mutations, and as maintenance therapy for recurrent platinum sensitive ovarian cancer (BRCA wild-type or mutated) after treatment with platinum. Platinum 174-182 poly(ADP-ribose) polymerase 1 Homo sapiens 30-34 31534014-1 2020 Poly (ADP-ribose) Polymerase (PARP) inhibitors (PARPi) are approved to treat recurrent ovarian cancer with BRCA1 or BRCA2 mutations, and as maintenance therapy for recurrent platinum sensitive ovarian cancer (BRCA wild-type or mutated) after treatment with platinum. Platinum 257-265 poly(ADP-ribose) polymerase 1 Homo sapiens 0-28 31534014-1 2020 Poly (ADP-ribose) Polymerase (PARP) inhibitors (PARPi) are approved to treat recurrent ovarian cancer with BRCA1 or BRCA2 mutations, and as maintenance therapy for recurrent platinum sensitive ovarian cancer (BRCA wild-type or mutated) after treatment with platinum. Platinum 257-265 poly(ADP-ribose) polymerase 1 Homo sapiens 30-34 31594824-7 2020 In addition, the levels and patterns of ADPRylation, PARP-1 protein, and gene expression correlated with clinical outcomes in response to platinum-based chemotherapy, with cancers exhibiting the highest levels of ADPRylation having the best outcomes independent of BRCA1/2 status. Platinum 138-146 poly(ADP-ribose) polymerase 1 Homo sapiens 53-59 31907114-4 2019 Vera, which can reverse chemotherapy resistance of tumor cells, showed no simple correlations with oxaliplatin drug resistance or P-gP expression and could enhance the anti-tumor effect of platinum chemotherapeutic agents by influencing the PARP pathway. Platinum 189-197 poly(ADP-ribose) polymerase 1 Homo sapiens 241-245 31629204-0 2019 Parp inhibitors as maintenance treatment in platinum sensitive recurrent ovarian cancer: An updated meta-analysis of randomized clinical trials according to BRCA mutational status. Platinum 44-52 poly(ADP-ribose) polymerase 1 Homo sapiens 0-4 31685558-1 2019 OBJECTIVE: To report results from an integrated efficacy and safety analysis supporting the European Commission"s approval of the poly(ADP-ribose) polymerase inhibitor rucaparib as monotherapy treatment for relapsed, platinum-sensitive, BRCA-mutated ovarian cancer. Platinum 217-225 poly(ADP-ribose) polymerase 1 Homo sapiens 130-157 31194214-0 2019 Immune Checkpoint and Poly(ADP-Ribose) Polymerase Inhibition for Recurrent Platinum-Resistant Ovarian and Metastatic Triple-Negative Breast Cancers. Platinum 75-83 poly(ADP-ribose) polymerase 1 Homo sapiens 22-49 31091037-6 2019 For tubo-ovarian cancers, the concept of << platinum-sensitive >> has been tempered since the arrival of antiangiogenic treatment and PARP inhibitors that prolong the disease control not only in patients with BRCA1/2 mutation, but also in others. Platinum 50-58 poly(ADP-ribose) polymerase 1 Homo sapiens 146-150 29961768-1 2019 PURPOSE: Germline variants in double-strand DNA damage repair (dsDDR) genes (e.g., BRCA1/2) predispose to pancreatic adenocarcinoma (PDAC) and may predict sensitivity to platinum-based chemotherapy and poly(ADP) ribose polymerase (PARP) inhibitors. Platinum 170-178 poly(ADP-ribose) polymerase 1 Homo sapiens 202-229 30797591-1 2019 PURPOSE: PARP inhibitor maintenance therapy in platinum sensitive sporadic ovarian cancers improves progression free survival. Platinum 47-55 poly(ADP-ribose) polymerase 1 Homo sapiens 9-13 30672100-3 2019 Homologous recombination deficiency (HRD) and platinum sensitivity are prospective biomarkers for predicting the response to PARP inhibitors in ovarian cancers. Platinum 46-54 poly(ADP-ribose) polymerase 1 Homo sapiens 125-129 30919167-4 2019 These defects confer increased sensitivity to platinum chemotherapy or poly (ADP-ribose) polymerase (PARP) inhibitors. Platinum 46-54 poly(ADP-ribose) polymerase 1 Homo sapiens 101-105 30540581-2 2019 RECENT FINDINGS: PARP inhibitors have been most studied in patients with breast and ovarian cancers associated with deleterious germline BRCA1 or BRCA2 mutations, though their role has expanded to include use as maintenance therapy in women with platinum-sensitive high-grade serous ovarian cancer due to the high propensity of such cancers to have defects in DNA repair by homologous recombination. Platinum 246-254 poly(ADP-ribose) polymerase 1 Homo sapiens 17-21 29961768-1 2019 PURPOSE: Germline variants in double-strand DNA damage repair (dsDDR) genes (e.g., BRCA1/2) predispose to pancreatic adenocarcinoma (PDAC) and may predict sensitivity to platinum-based chemotherapy and poly(ADP) ribose polymerase (PARP) inhibitors. Platinum 170-178 poly(ADP-ribose) polymerase 1 Homo sapiens 231-235 30228165-5 2018 OCs driven by BRCA1/2, FA-associated, and BRCAness germline mutations have a demonstrated sensitivity to PARP inhibitors due to underlying deficiencies in DNA homologous recombination; however, clinical responses are often partial and highly dependent on platinum sensitivity. Platinum 255-263 poly(ADP-ribose) polymerase 1 Homo sapiens 105-109 30278221-0 2018 PARP inhibition in platinum-based chemotherapy: Chemopotentiation and neuroprotection. Platinum 19-27 poly(ADP-ribose) polymerase 1 Homo sapiens 0-4 30278221-6 2018 Inhibition of poly(ADP-ribose) polymerase (PARP), a nuclear enzyme activated upon DNA damage, has demonstrated substantial sensory and enteric neuroprotective capacity when administered in combination with platinum chemotherapeutics. Platinum 206-214 poly(ADP-ribose) polymerase 1 Homo sapiens 14-41 30278221-6 2018 Inhibition of poly(ADP-ribose) polymerase (PARP), a nuclear enzyme activated upon DNA damage, has demonstrated substantial sensory and enteric neuroprotective capacity when administered in combination with platinum chemotherapeutics. Platinum 206-214 poly(ADP-ribose) polymerase 1 Homo sapiens 43-47 30080919-4 2018 More recently, these two and a third PARP inhibitor, niraparib, were approved by the FDA as maintenance therapy following platinum-based chemotherapy for recurrent ovarian cancer. Platinum 122-130 poly(ADP-ribose) polymerase 1 Homo sapiens 37-41 29871906-2 2018 PARP inhibitors are now approved for recurrent ovarian cancer as maintenance following response to platinum chemotherapy and BRCA-mutated (BRCAm) cancer treatment. Platinum 99-107 poly(ADP-ribose) polymerase 1 Homo sapiens 0-4 30082520-9 2018 Conclusions: The PARP1 2444 mutation allele C might be associated with the decreased sensitivity to platinum-based chemotherapy in advanced NSCLC. Platinum 100-108 poly(ADP-ribose) polymerase 1 Homo sapiens 17-22 29396858-8 2018 Correlation between disease course at tissue acquisition and response to PARP inhibitor (PARPi)/platinum was demonstrated in PDXs in vivo. Platinum 96-104 poly(ADP-ribose) polymerase 1 Homo sapiens 73-77 29232464-11 2017 The presence of germline or somatic BRCA mutations allows platinum-responsive patients to optimize chemotherapy efficacy and prolonging PFS by the use of olaparib (PARP inhibitor) given as maintenance therapy until progression. Platinum 58-66 poly(ADP-ribose) polymerase 1 Homo sapiens 164-168 29750420-3 2018 We review key trials that have led to the approval of three PARP inhibitors-olaparib, niraparib and rucaparib-as maintenance therapy for platinum-sensitive recurrent ovarian cancer. Platinum 137-145 poly(ADP-ribose) polymerase 1 Homo sapiens 60-64 29750420-6 2018 Three phase III trials (NOVA, SOLO2 and ARIEL3) demonstrated remarkable improvement in progression-free survival (PFS) with PARP inhibitors given as maintenance therapy in patients with complete or partial response after platinum-based therapy for platinum-sensitive ovarian cancer. Platinum 221-229 poly(ADP-ribose) polymerase 1 Homo sapiens 124-128 30067614-7 2018 PARP inhibitors, which inhibit DNA repair, have shown the greatest activity in those ovarian cancers that harbor deleterious BRCA mutations, and they have also demonstrated activity in the maintenance setting after a response to and completion of platinum-based chemotherapy in patients with sensitive recurrent ovarian cancer regardless of BRCA status. Platinum 247-255 poly(ADP-ribose) polymerase 1 Homo sapiens 0-4 29397193-1 2018 Niraparib is an oral poly(ADP ribose) polymerase (PARP) inhibitor that is currently approved by the United States Food and Drug Administration (US FDA) as well as recently approved by the European Medicines Agency (EMA) for the maintenance treatment of women with recurrent ovarian cancer who are in complete or partial response to platinum-based chemotherapy. Platinum 332-340 poly(ADP-ribose) polymerase 1 Homo sapiens 50-54 29109859-1 2017 Inhibitors of poly(ADP-ribose) polymerase (PARP) are new types of personalized treatment of relapsed platinum-sensitive ovarian cancer harboring BRCA1/2 mutations. Platinum 101-109 poly(ADP-ribose) polymerase 1 Homo sapiens 14-41 29109859-1 2017 Inhibitors of poly(ADP-ribose) polymerase (PARP) are new types of personalized treatment of relapsed platinum-sensitive ovarian cancer harboring BRCA1/2 mutations. Platinum 101-109 poly(ADP-ribose) polymerase 1 Homo sapiens 43-47 28487881-3 2017 This would not have been detected by standard BRCA testing, and it led to additional treatment with a maintenance poly ADP ribose polymerase (PARP) inhibitor following platinum-based chemotherapy. Platinum 168-176 poly(ADP-ribose) polymerase 1 Homo sapiens 114-140 28471247-2 2017 Areas covered: This review focuses on the main hematologic and non-hematologic toxicities correlated with the use of licensed antiangiogenic agents and PARP inhibitors in recurrent platinum-sensitive EOC, providing recommendations for their management. Platinum 181-189 poly(ADP-ribose) polymerase 1 Homo sapiens 152-156 28487881-3 2017 This would not have been detected by standard BRCA testing, and it led to additional treatment with a maintenance poly ADP ribose polymerase (PARP) inhibitor following platinum-based chemotherapy. Platinum 168-176 poly(ADP-ribose) polymerase 1 Homo sapiens 142-146 27821802-4 2016 Homologous Recombination deficiency has been assumed to be a Germ Cell Tumor characteristic underlying platinum-sensitivity, whereby Poly(ADP-ribose) polymerase (PARP), an enzyme involved in HR DNA repair, is an intriguing target: PARP inhibitors have already entered in clinical practice of other malignancies and trials are recruiting TGCT patients in order to validate their role in this disease. Platinum 103-111 poly(ADP-ribose) polymerase 1 Homo sapiens 133-160 27655641-6 2016 We also demonstrated that silencing PARP1 enhanced the cell death induced by the platinum-based chemotherapy drug carboplatin in lung cancer cells (CL1-5 and H1975). Platinum 81-89 poly(ADP-ribose) polymerase 1 Homo sapiens 36-41 27884198-5 2016 The PARP inhibitor Olaparib [AZD2281] has been approved by the FDA for use in pretreated ovarian cancer patients with defective BRCA1/2 genes, and by the EMEA for maintenance therapy in platinum sensitive ovarian cancer patients with defective BRCA1/2 genes. Platinum 186-194 poly(ADP-ribose) polymerase 1 Homo sapiens 4-8 27736844-6 2016 PARP inhibitors have demonstrated durable antitumour activity in BRCA-mutated advanced OC as a single agent in the treatment and maintenance setting, particularly in platinum-sensitive disease. Platinum 166-174 poly(ADP-ribose) polymerase 1 Homo sapiens 0-4 27756336-1 2016 BACKGROUND: Triple-negative breast cancer (TNBC) with a BRCA1-like molecular signature has been demonstrated to remarkably respond to platinum-based chemotherapy and might be suited for a future treatment with poly(ADP-ribose)polymerase (PARP) inhibitors. Platinum 134-142 poly(ADP-ribose) polymerase 1 Homo sapiens 210-236 27756336-1 2016 BACKGROUND: Triple-negative breast cancer (TNBC) with a BRCA1-like molecular signature has been demonstrated to remarkably respond to platinum-based chemotherapy and might be suited for a future treatment with poly(ADP-ribose)polymerase (PARP) inhibitors. Platinum 134-142 poly(ADP-ribose) polymerase 1 Homo sapiens 238-242 27155850-6 2016 High PARP activity was associated with platinum sensitivity both in the entire study cohort (p = 0.022) and in the high-grade subgroup (p = 0.017). Platinum 39-47 poly(ADP-ribose) polymerase 1 Homo sapiens 5-9 27155850-9 2016 In conclusion, we present a novel finding of high PARP activity associated with platinum sensitivity and improved PFS in EOC. Platinum 80-88 poly(ADP-ribose) polymerase 1 Homo sapiens 50-54 27127105-5 2016 More research is needed to assesses whether inhibitors of PARP have any role as maintenance treatment after first-line chemotherapy and as palliative treatment of platinum-resistant disease. Platinum 163-171 poly(ADP-ribose) polymerase 1 Homo sapiens 58-62 26984416-2 2016 Demonstration of anti-cancer activity has led to the European Medicines Agency (EMA) approval of the PARP inhibitor (PARPi) olaparib as maintenance therapy in women with BRCA-mutated (BRCAm) ovarian cancer with platinum-sensitive recurrence following response to platinum therapy and the US Food and Drug Administration (US FDA) approval of olaparib in relapsed germline BRCA-mutated (gBRCAm) ovarian cancer in women who have received at least three prior chemotherapy treatments, both occurring in 2014. Platinum 211-219 poly(ADP-ribose) polymerase 1 Homo sapiens 101-105 26984416-2 2016 Demonstration of anti-cancer activity has led to the European Medicines Agency (EMA) approval of the PARP inhibitor (PARPi) olaparib as maintenance therapy in women with BRCA-mutated (BRCAm) ovarian cancer with platinum-sensitive recurrence following response to platinum therapy and the US Food and Drug Administration (US FDA) approval of olaparib in relapsed germline BRCA-mutated (gBRCAm) ovarian cancer in women who have received at least three prior chemotherapy treatments, both occurring in 2014. Platinum 263-271 poly(ADP-ribose) polymerase 1 Homo sapiens 101-105 26693899-10 2016 Nevertheless, all primary platinum-sensitive HGSOCs remained HR-deficient, irrespective of whether they became resistant to second-line platinum, further suggesting these tumours qualify for second-line Poly APD ribose polymerase (PARP) inhibitor treatment. Platinum 26-34 poly(ADP-ribose) polymerase 1 Homo sapiens 231-235 26206420-8 2015 Studies are also being undertaken with inhibitors of poly(ADP-ribose) polymerase (PARP), targeting the DNA repair pathway as it is possible that the benefits seen with these agents in "platinum-sensitive" disease will apply to those with "platinum-resistant" disease. Platinum 185-193 poly(ADP-ribose) polymerase 1 Homo sapiens 53-80 26669450-8 2015 Based on the evidence presented, patients who will receive the greatest benefit from PARP inhibition are those with platinum-sensitive relapsed ovarian cancer and a BRCA mutation. Platinum 116-124 poly(ADP-ribose) polymerase 1 Homo sapiens 85-89 26646960-6 2015 The PARP inhibitor olaparib is recommended as maintenance treatment of women with platinum sensitive relapsed BRCA mutated high-grade serous EOC who have responded to platinum-based chemotherapy. Platinum 82-90 poly(ADP-ribose) polymerase 1 Homo sapiens 4-8 26269716-6 2015 We found that IL6, TNF, CXCL8, IL1B and ERK1/2 were the top genes in terms of the number of connections in platinum-induced neuropathy and TP53, MYC, PARP1, P38 MAPK and TNF for combined taxane-platinum-induced neuropathy. Platinum 107-115 poly(ADP-ribose) polymerase 1 Homo sapiens 150-155 25304989-4 2015 Recent reports have suggested that in the setting of impaired DNA repair, chemotherapeutic agents that induce DNA damage, such as platinum-based antineoplastic drugs (platins) and poly(ADP-ribose) polymerase inhibitors (PARP inhibitors), have improved efficacy. Platinum 130-138 poly(ADP-ribose) polymerase 1 Homo sapiens 220-224 25991068-19 2015 AUTHORS" CONCLUSIONS: PARP inhibitors appear to improve PFS in women with recurrent platinum-sensitive disease. Platinum 84-92 poly(ADP-ribose) polymerase 1 Homo sapiens 22-26 25779564-1 2015 Poly (ADP-ribose) polymerase (PARP) inhibitors have shown promising activity in epithelial ovarian cancers, especially relapsed platinum-sensitive high-grade serous disease. Platinum 128-136 poly(ADP-ribose) polymerase 1 Homo sapiens 0-28 25779564-1 2015 Poly (ADP-ribose) polymerase (PARP) inhibitors have shown promising activity in epithelial ovarian cancers, especially relapsed platinum-sensitive high-grade serous disease. Platinum 128-136 poly(ADP-ribose) polymerase 1 Homo sapiens 30-34 26206420-8 2015 Studies are also being undertaken with inhibitors of poly(ADP-ribose) polymerase (PARP), targeting the DNA repair pathway as it is possible that the benefits seen with these agents in "platinum-sensitive" disease will apply to those with "platinum-resistant" disease. Platinum 185-193 poly(ADP-ribose) polymerase 1 Homo sapiens 82-86 26206420-8 2015 Studies are also being undertaken with inhibitors of poly(ADP-ribose) polymerase (PARP), targeting the DNA repair pathway as it is possible that the benefits seen with these agents in "platinum-sensitive" disease will apply to those with "platinum-resistant" disease. Platinum 239-247 poly(ADP-ribose) polymerase 1 Homo sapiens 53-80 26206420-8 2015 Studies are also being undertaken with inhibitors of poly(ADP-ribose) polymerase (PARP), targeting the DNA repair pathway as it is possible that the benefits seen with these agents in "platinum-sensitive" disease will apply to those with "platinum-resistant" disease. Platinum 239-247 poly(ADP-ribose) polymerase 1 Homo sapiens 82-86 26374559-10 2015 Some resistant cancer cells continue to respond to platinum based drugs, encouraging further development of PARP inhibitors for cancer treatment. Platinum 51-59 poly(ADP-ribose) polymerase 1 Homo sapiens 108-112 25124282-5 2014 Mechanisms of differential sensitivity of SCLC cell lines to PARP inhibition were investigated by comparing protein and gene expression profiles of the platinum sensitive and the less sensitive cell lines. Platinum 152-160 poly(ADP-ribose) polymerase 1 Homo sapiens 61-65 24607283-5 2014 Pending review by the Food and Drug Administration (FDA) and the outcome of confirmatory phase III studies, PARP inhibitors could become the first FDA-approved biologic agent for ovarian cancer and also the first new FDA-approval in ovarian cancer since carboplatin and gemcitabine were approved for platinum sensitive ovarian cancer in 2006. Platinum 300-308 poly(ADP-ribose) polymerase 1 Homo sapiens 108-112 24761869-0 2014 Expression of ERCC1, MSH2 and PARP1 in non-small cell lung cancer and prognostic value in patients treated with platinum-based chemotherapy. Platinum 112-120 poly(ADP-ribose) polymerase 1 Homo sapiens 30-35 24761869-9 2014 CONCLUSION: Patients with ERCC1 or PARP1 negative non-small cell lung cancer appear to benefit from platinum-based postoperative adjuvant chemotherapy. Platinum 100-108 poly(ADP-ribose) polymerase 1 Homo sapiens 35-40 24189460-7 2014 Furthermore, PARP-1 mutant overexpression in a pancreatic cancer cell line (MIA PaCa-2) increased sensitivity to platinum-based anticancer agents. Platinum 113-121 poly(ADP-ribose) polymerase 1 Homo sapiens 13-19 24361480-2 2014 Here we describe a strategy to conveniently obtain metal-based PARP-1 inhibitors with enhanced biological activities by conjugating platinum moiety with an original inhibitor, e.g., benzonaphthyridone. Platinum 132-140 poly(ADP-ribose) polymerase 1 Homo sapiens 63-69 24361480-7 2014 Our study implies that the conjugation of platinum with PARP-1 inhibitors could be a valid strategy to obtain more potent anticancer agents with improved biological activities. Platinum 42-50 poly(ADP-ribose) polymerase 1 Homo sapiens 56-62 22869732-1 2012 Expression of functional breast cancer susceptibility gene 1 (BRCA1) in human breast and ovarian cancers is associated with resistance to platinum-based chemotherapeutics and poly(ADP ribose) polymerase (PARP) inhibitors. Platinum 138-146 poly(ADP-ribose) polymerase 1 Homo sapiens 175-202 23275151-4 2013 Therefore, we hypothesized that combining PARP inhibition with platinum compounds may be an approach to improve platinum-based therapy for NSCLC. Platinum 112-120 poly(ADP-ribose) polymerase 1 Homo sapiens 42-46 22983827-0 2013 Association between polymorphisms of XRCC1 and ADPRT genes and ovarian cancer survival with platinum-based chemotherapy in Chinese population. Platinum 92-100 poly(ADP-ribose) polymerase 1 Homo sapiens 47-52 22983827-2 2013 We conducted a prospective study to determine whether associations exist between two polymorphisms in XRCC1 and ADPRT and the outcomes of Chinese ovarian cancer patients treated with platinum-based chemotherapy. Platinum 183-191 poly(ADP-ribose) polymerase 1 Homo sapiens 112-117 22926640-10 2012 A PARP inhibitor, olaparib, applied as maintenance treatment also improved PFS in platinum-sensitive relapsed ovarian cancer. Platinum 82-90 poly(ADP-ribose) polymerase 1 Homo sapiens 2-6 23479135-8 2013 CONCLUSIONS: We found that XRCC1 Arg399Gln, PARP1 Va1762Ala and APE1 Asp148Glu SNPs in the BER pathway may influence the prognosis of advanced NSCLC patients following platinum-based chemotherapy. Platinum 168-176 poly(ADP-ribose) polymerase 1 Homo sapiens 44-49 23410825-0 2013 PARP1 impact on DNA repair of platinum adducts: preclinical and clinical read-outs. Platinum 30-38 poly(ADP-ribose) polymerase 1 Homo sapiens 0-5 23410825-7 2013 Further, the pharmacological inhibition of PARP induced a 1.7 to 2.3-fold increase in platinum adduct accumulation (24h) in A549 cell line suggesting a slow-down of platinum DNA-adduct repair capacity. Platinum 86-94 poly(ADP-ribose) polymerase 1 Homo sapiens 43-47 23410825-7 2013 Further, the pharmacological inhibition of PARP induced a 1.7 to 2.3-fold increase in platinum adduct accumulation (24h) in A549 cell line suggesting a slow-down of platinum DNA-adduct repair capacity. Platinum 165-173 poly(ADP-ribose) polymerase 1 Homo sapiens 43-47 23410825-13 2013 In conclusion, our data confirm that platinum DNA adduct accumulation is linked to chemosensitivity, which increase by pharmacological PARP inhibitors points to a role of PARP-dependent DNA repair in the process. Platinum 37-45 poly(ADP-ribose) polymerase 1 Homo sapiens 135-139 23410825-13 2013 In conclusion, our data confirm that platinum DNA adduct accumulation is linked to chemosensitivity, which increase by pharmacological PARP inhibitors points to a role of PARP-dependent DNA repair in the process. Platinum 37-45 poly(ADP-ribose) polymerase 1 Homo sapiens 171-175 23640560-9 2013 The RT-PCR analysis revealed that the expression of PARP-1 mRNA was decreased when platinum (Pt) and 3-AB were combined. Platinum 83-91 poly(ADP-ribose) polymerase 1 Homo sapiens 52-58 23640560-9 2013 The RT-PCR analysis revealed that the expression of PARP-1 mRNA was decreased when platinum (Pt) and 3-AB were combined. Platinum 93-95 poly(ADP-ribose) polymerase 1 Homo sapiens 52-58 22869732-1 2012 Expression of functional breast cancer susceptibility gene 1 (BRCA1) in human breast and ovarian cancers is associated with resistance to platinum-based chemotherapeutics and poly(ADP ribose) polymerase (PARP) inhibitors. Platinum 138-146 poly(ADP-ribose) polymerase 1 Homo sapiens 204-208 18977144-0 2008 Poly(ADP-ribose) polymerase-1 activity facilitates the dissociation of nuclear proteins from platinum-modified DNA. Platinum 93-101 poly(ADP-ribose) polymerase 1 Homo sapiens 0-29 22504675-5 2012 Inhibition of PARP potentiates the activity of DNA-damaging agents, such as alkylators, platinums, topoisomerase inhibitors, and radiation both in vitro and in vivo. Platinum 88-97 poly(ADP-ribose) polymerase 1 Homo sapiens 14-18 21819606-2 2011 Breast and ovarian neoplasms from BRCA1 or BRCA2 mutation carriers are characterized by deficient homologous recombination (HR) of DNA, that makes them particularly sensitive to platinum compounds or inhibitors of poly (ADP-ribose) polymerase (PARP). Platinum 178-186 poly(ADP-ribose) polymerase 1 Homo sapiens 244-248 21370912-1 2011 The inhibition activity of a series of anticancer metal complexes based on platinum, ruthenium, and gold metal ions was evaluated on the zinc-finger protein PARP-1, either purified or directly on protein extracts from human breast cancer MCF7 cells. Platinum 75-83 poly(ADP-ribose) polymerase 1 Homo sapiens 157-163 20550106-0 2010 Recognition of platinum-DNA damage by poly(ADP-ribose) polymerase-1. Platinum 15-23 poly(ADP-ribose) polymerase 1 Homo sapiens 38-67 20550106-2 2010 To investigate the properties of binding of PARP-1 to different platinum-DNA adducts in greater detail, biotinylated DNA probes containing a site-specific cisplatin 1,2-d(GpG) or 1,3-d(GpTpG) intrastrand cross-link or a cisplatin 5"-GC/5"-GC interstrand cross-link (ICL) were utilized in binding assays with cell-free extracts (CFEs) in vitro. Platinum 64-72 poly(ADP-ribose) polymerase 1 Homo sapiens 44-50 20550106-6 2010 The role of poly(ADP-ribose) (pADPr) in mediating binding of PARP-1 to platinum damage was further investigated. Platinum 71-79 poly(ADP-ribose) polymerase 1 Homo sapiens 61-67 20550106-9 2010 PARP-1 also binds to DNA damaged by other platinum compounds, including oxaliplatin and pyriplatin, indicating protein affinity for the damage in an adduct-specific manner rather than recognition of distorted DNA. Platinum 42-50 poly(ADP-ribose) polymerase 1 Homo sapiens 0-6 20550106-10 2010 Our results reveal the unique binding properties for binding of PARP-1 to platinum-DNA damage, providing insights into, and a better understanding of, the cellular response to platinum-based anticancer drugs. Platinum 74-82 poly(ADP-ribose) polymerase 1 Homo sapiens 64-70 20550106-10 2010 Our results reveal the unique binding properties for binding of PARP-1 to platinum-DNA damage, providing insights into, and a better understanding of, the cellular response to platinum-based anticancer drugs. Platinum 176-184 poly(ADP-ribose) polymerase 1 Homo sapiens 64-70 20940192-6 2010 CONCLUSION: Polymorphisms in the TP53 and PARP1 genes are involved in inter-individual differences in the response to platinum-based doublet chemotherapy in patients with NSCLC. Platinum 118-126 poly(ADP-ribose) polymerase 1 Homo sapiens 42-47 20406929-0 2010 Poly(ADP)-ribose polymerase inhibition: frequent durable responses in BRCA carrier ovarian cancer correlating with platinum-free interval. Platinum 115-123 poly(ADP-ribose) polymerase 1 Homo sapiens 0-27 19053130-9 2009 The affinity of PARP-1 for platinum-modified DNA was established using this type of probe for the first time. Platinum 27-35 poly(ADP-ribose) polymerase 1 Homo sapiens 16-22 18977144-1 2008 The affinity of the poly(ADP-ribose) polymerase-1 (PARP-1) for platinum-damaged DNA was first discovered during photo-cross-linking experiments using the photoactive compound Pt-BP6 [J. Platinum 63-71 poly(ADP-ribose) polymerase 1 Homo sapiens 20-49 18977144-1 2008 The affinity of the poly(ADP-ribose) polymerase-1 (PARP-1) for platinum-damaged DNA was first discovered during photo-cross-linking experiments using the photoactive compound Pt-BP6 [J. Platinum 63-71 poly(ADP-ribose) polymerase 1 Homo sapiens 51-57 18977144-7 2008 We find that the activity of PARP proteins following exposure to platinum-modified DNA results in the dissociation of DNA-bound proteins. Platinum 65-73 poly(ADP-ribose) polymerase 1 Homo sapiens 29-33 17332279-3 2007 Inhibition of PARP potentiates the activity of DNA-damaging agents, such as alkylators, platinums, topoisomerase inhibitors, and radiation in in vitro and in vivo models. Platinum 88-97 poly(ADP-ribose) polymerase 1 Homo sapiens 14-18 16787355-4 2006 In the present study we report that PARP-1 inhibitor 3-aminobenzamide (3-AB) increases the cytotoxic activity of the platinum compounds cisplatin, trans-[PtCl(2)(4-picoline)(piperazine)] and transplatin against CH1cisR cisplatin-resistant ovarian tumor cells. Platinum 117-125 poly(ADP-ribose) polymerase 1 Homo sapiens 36-42 16787355-6 2006 Altogether, these data suggest that pharmacological modulation of PARP-1 by inhibitors may be a suitable strategy to fight against tumor resistance to platinum drugs. Platinum 151-159 poly(ADP-ribose) polymerase 1 Homo sapiens 66-72