ライフサイエンスコーパス: PARP Inhibitor

1 (BER) and formation of DPCs is enhanced by a PARP inhibitor.

2 to the TNFRSF10B promoter in the presence of PARP inhibitor.

3 y, to predict response to rucaparib, an oral PARP inhibitor.

4 ose deposition in the presence of a chemical PARP inhibitor.

5 n with poly(ADP-ribose) glycohydrolase and a PARP inhibitor.

6 decrease was almost completely blocked by a PARP inhibitor.

7 most likely to respond therapeutically to a PARP inhibitor.

8 has important implications for the design of PARP inhibitors.

9 may benefit from either platinum therapy or PARP inhibitors.

10 at may be useful therapeutic alternatives to PARP inhibitors.

11 fficient for patients to derive benefit from PARP inhibitors.

12 implications for the mechanism of action of Parp inhibitors.

13 hese pathological changes were attenuated by PARP inhibitors.

14 immunotherapy combined with chemotherapy and PARP inhibitors.

15 of EOC patients that is likely to respond to PARP inhibitors.

16 e repair underlies responses to platinum and PARP inhibitors.

17 ble to the synthetic lethal combination with PARP inhibitors.

18 and confer resistance to platinum salts and PARP inhibitors.

19 motherapy and may also predict resistance to PARP inhibitors.

20 otoxicity in HR-deficient cells treated with PARP inhibitors.

21 ert therapeutic activity in combination with PARP inhibitors.

22 he cytotoxicity of two structurally distinct PARP inhibitors.

23 monstrates reduced HDR in cells treated with PARP inhibitors.

24 correlated with an increased sensitivity to PARP inhibitors.

25 for biomarker studies in clinical trials of PARP inhibitors.

26 u80 defective cells shown to be sensitive to PARP inhibitors.

27 /BRCA2) also confer selective sensitivity to PARP inhibitors.

28 PN cells to synthetic lethality triggered by PARP inhibitors.

29 xic sensitivity of cell lines evaluated with PARP inhibitors.

30 e maintenance and regulating the efficacy of PARP inhibitors.

31 s to DNA damaging therapeutic agents such as PARP inhibitors.

32 ithelial cells and to enhance sensitivity to PARP inhibitors.

33 ted as a potent poly(ADP-ribose) polymerase (PARP) inhibitor.

34 lomestatin or a poly(ADP ribose) polymerase (PARP) inhibitor.

35 re sensitive to poly(ADP-ribose) polymerase (PARP) inhibitors.

36 ly(adenosine diphosphate ribose) polymerase (PARP) inhibitors.

37 herapeutics and poly(ADP ribose) polymerase (PARP) inhibitors.

38 ranslocation to poly(ADP-ribose) polymerase (PARP) inhibitors.

39 emotherapy and poly (ADP-ribose) polymerase (PARP) inhibitors.

40 ly sensitive to poly(ADP-ribose) polymerase (PARP) inhibitors.

41 ent tumours to poly-ADP-ribose polymerase-1 (PARP) inhibitors.

42 inum drugs and poly (ADP-ribose) polymerase (PARP) inhibitors.

43 r exacerbated by poly-ADP ribose polymerase (PARP) inhibitors.

44 g cisplatin and poly(ADP-ribose) polymerase (PARP) inhibitors.

45 abetic rats were treated with or without the PARP inhibitors 1,5-isoquinolinediol (ISO; 3 mg kg(-1) d

46 ll death that was inhibited by PJ34 and DPQ, PARP inhibitors, 2-APB, a TRPM2 channel inhibitor, and p

47 RP-1-/- microglia and in wt microglia by the PARP inhibitor 3,4-dihydro-5-[4-(1-piperidinyl)butoxy]-1

48 oic acid) porphyrin chloride (MnTBAP) or the PARP inhibitor 3-aminobenzamide (3-AB).

49 This effect could be reversed with the PARP inhibitor 3-aminobenzamide and did not occur in cel

50 Importantly, the PARP inhibitor 3-aminobenzamide enhanced macrophage ABCA

51 but not by the poly (ADP-ribose) polymerase (PARP) inhibitor 3-aminobenzamide (3-AB).

52 Two structurally unrelated PARP inhibitors, 3-aminobenzamide and 1,5-isoquinolinedi

53 onversely that AT cells are sensitive to the PARP inhibitor 4-amino-1,8-napthalamide.

54 sly discovered by our group and a congeneric PARP inhibitor, a library of derivatives was synthesized

55 In a B16F10 mouse syngeneic tumor model, PARP inhibitor ABT-888 potentiates the effect of temozol

56 In vivo, the clinically available PARP inhibitor ABT-888 reversed PAH in 2 experimental ra

57 ufficient to render cells susceptible to the PARP inhibitors ABT-888 and AZD-2281 both in vitro and i

58 ensitive to the poly(ADP-ribose) polymerase (PARP) inhibitor ABT-888 due to synthetic lethality.

59 n study of the poly (ADP-ribose) polymerase (PARP) inhibitor ABT-888 in patients with advanced malign

60 ER pathway, the poly(ADP-ribose) polymerase (PARP) inhibitors ABT-888 (veliparib) and AZD2281 (olapar

61 We show a mechanistic interaction of a PARP inhibitor, ABT-888, with a topoisomerase I inhibito

62 Bs caused by PARP inactivation, arguing that PARP inhibitors act in part as poisons that trap PARP en

63 vide a molecular framework for understanding PARP inhibitor action and, more generally, allosteric co

64 , these observations identify a new facet of PARP inhibitor action while simultaneously providing the

65 used to assess the therapeutic potential of PARP inhibitors after hypoglycemia.

66 platin and to a poly(ADP-ribose) polymerase (PARP) inhibitor (AG14361).

67 ion of the pS516 CHK2 signal was seen with a PARP inhibitor alone, and this activation was abolished

68 more, OGG1(-/-) cells were more sensitive to PARP inhibitors alone or in combination with a DNA-damag

69 PARP inhibitors also attenuated the development of BDL-i

70 ling of the PARP3-active site with different PARP inhibitors also highlights the potential to develop

71 When PARP inhibitors and beta-lapachone are combined, synergi

72 -selective, caspase-dependent apoptosis with PARP inhibitors and beta-lapachone.

73 residual tumors that are radiosensitized by PARP inhibitors and chemotherapy.

74 More generally, acquisition of PARP inhibitors and cisplatin resistance is associated w

75 We profiled 10 clinical PARP inhibitors and commonly used research tools for the

76 rrelates with responsiveness to platinum and PARP inhibitors and identifies a subset of sporadic pati

77 Here, we discuss current knowledge of PARP inhibitors and potential ways to maximize their cli

78 ing agents, to Poly (ADP-ribose) polymerase (PARP) inhibitors and cross-linking agents and inhibits t

79 ([Ca(2+)]c), which was inhibited by PJ34, a PARP inhibitor, and abolished by TRPM2 knockout (TRPM2-K

80 in clinical trials, such as mTOR inhibitors, PARP inhibitors, and CDK4/6 inhibitors.

81 with genotoxic chemotherapeutics, including PARP inhibitors, and nongenotoxic activation of p53.

82 We further show that PARP inhibitors, and Parp-1 knockdown by siRNA induce Bc

83 PARP1 pY907 may predict tumor resistance to PARP inhibitors, and that treatment with a combination o

84 Several PARP inhibitors appear to be additive to synergistic wit

85 neration agent following olaparib, the first PARP inhibitor approved for cancer therapy.

86 PARP inhibitors are an exciting new class of targeted th

87 PARP inhibitors are currently being used in clinical tri

88 PARP inhibitors are currently in clinical trials for onc

89 Moreover, PARP inhibitors are emerging as anti-cancer drugs in pha

90 Because PARP inhibitors are not cytotoxic, a biomarker assay is

91 As such, PARP inhibitors are promising new therapies for repair-d

92 Poly(ADP-ribose) polymerase (PARP) inhibitors are strikingly toxic to cells with defe

93 ial for RAD51 focus formation, and conferred PARP inhibitor as well as cisplatin resistance.

94 bition together give the same sensitivity to PARP inhibitors as ATM alone, indicating that ATM functi

95 teins (PAR(high)) responded to pharmacologic PARP inhibitors as well as to PARP1-targeting siRNAs by

96 ecombination and enhanced sensitivity to the PARP inhibitor AZD2281 in vitro and to cisplatin both in

97 silenced cause synthetic lethality with the PARP inhibitor AZD2281.

98 The PARP inhibitor AZD2461 was developed as a next-generatio

99 tance could be circumvented by using another PARP inhibitor, AZD2461, which is a poor Pgp substrate.

100 lso required, since transient application of PARP inhibitors blocked LTF.

101 of hyperglycemia-induced PARP activation, as PARP inhibitors blocked the hyperglycemia-induced ROS ge

102 ersensitive to Poly (ADP ribose)-polymerase (PARP) inhibitors, but can acquire resistance and relapse

103 Resistance to PARP inhibitors can occur through genetic reversion in t

104 Poly(ADP-ribose) polymerase (PARP) inhibitors can generate synthetic lethality in can

105 CCT241533, implying that the potentiation of PARP inhibitor cell killing by CCT241533 was due to inhi

106 d increased sensitivity to both platinum and PARP inhibitor chemotherapy compared to Trp53 (-/-).

107 s not possess characteristics typical of the PARP inhibitor class, in combination with chemotherapy i

108 We provide an update on PARP inhibitor clinical development, describe recent adv

109 or veliparib, a poly(ADP-ribose) polymerase (PARP) inhibitor, combined with carboplatin.

110 Administration of PARP inhibitors confirms that poly(ADP-ribose) facilitat

111 CR-ABL1 to the combination of DNA ligase and PARP inhibitors correlates with the steady state levels

112 These data indicate that brain-permeable PARP inhibitors could effectively delay or prevent disea

113 RP) with ABT-888 (veliparib), one of several PARP inhibitors currently in clinical trials.

114 PARP inhibitors decreased diabetes-induced podocyte depl

115 Both PARP inhibitors delayed, but did not prevent, the format

116 Conversely, Sp1 knockdown diminished the PARP inhibitor effects.

117 ark for experimental design in assessment of PARP inhibitor effects.

118 Combinations of cisplatin or PARP inhibitors enhanced the antitumor cell effect of AT

119 This has led to PARP inhibitors entering clinical trials as a potential

120 DNA methylating agent in combination with a PARP inhibitor exhibit higher cytotoxicity than cells tr

121 PARP inhibitors exploit synthetic lethality to target DN

122 ient cells to a poly (ADP-ribose polymerase (PARP) inhibitor, expression of hLig151D did not, presuma

123 pair, including poly(ADP-ribose) polymerase (PARP) inhibitors, fail due to lack of tumor-selectivity.

124 ell lines showed an increased sensitivity to PARP inhibitors (Figure 4C).

125 utic treatments based on genotoxic agents or PARP inhibitors following a synthetic lethal strategy.

126 Despite the availability of PARP inhibitors for cancer therapy, a biomarker to clear

127 ograft models, expanding use and efficacy of PARP inhibitors for human cancer therapy.

128 s provide a rationale for the development of PARP inhibitors for the prevention of diabetic ocular co

129 Lynparza), the poly (ADP-ribose) polymerase (PARP) inhibitor for treating tumors harboring BRCA1 or B

130 Administration of PJ-34 (a potent PARP inhibitor) for 9 months to diabetic rats significan

131 Notably, concentrations of PARP inhibitor >1000-fold higher than the IC50 were requ

132 Olaparib, a poly(ADP-ribose) polymerase (PARP) inhibitor, has previously shown efficacy in a phas

133 Until now, numbers of PARP inhibitors have been reported and used for breast c

134 Therefore, novel antioxidants and PARP inhibitors have entered clinical development for th

135 Recently, several PARP inhibitors have entered clinical trials either as s

136 PARP inhibitors have gained recent attention due to thei

137 Poly(ADP-ribose) polymerase (PARP) inhibitors have activity in ovarian carcinomas wit

138 Poly (ADP-ribose) polymerase (PARP) inhibitors have emerged as promising cancer therap

139 Poly (ADP-ribose) polymerase (PARP) inhibitors have emerged as promising therapeutics

140 Poly (ADP-ribose) polymerase (PARP) inhibitors have shown promising activity in epithe

141 Poly (ADP-ribose) polymerase (PARP) inhibitors have shown promising results in clinica

142 eport discusses poly(ADP-ribose) polymerase (PARP) inhibitors, hedgehog inhibitors, and histone deace

143 DNA damage-induced poly(ADP-ribosyl)ation by PARP inhibitors impairs early DNA damage response events

144 Furthermore, chemical PARP inhibitors improve axon regeneration when administe

145 monstrate that this assay can readily detect PARP inhibitors in a high-throughput screen using 384-we

146 roup of patients who are PTEN deficient with PARP inhibitors in addition to the current treatment reg

147 rovide a preclinical rational for the use of PARP inhibitors in ATM-affected human CLL.ATM and TP53 m

148 evaluate ATR inhibitors in combination with PARP inhibitors in BRCA1/2-deficient cells.

149 c foundation for the rational application of PARP inhibitors in cancer therapy.

150 lly could be exploited therapeutically using PARP inhibitors in combination with androgen-deprivation

151 es the structure valuable for development of PARP inhibitors in general.

152 als have demonstrated promising responses to PARP inhibitors in pancreatic cancer patients.

153 e results extend the potential usefulness of PARP inhibitors in the treatment setting beyond BRCA mut

154 dence for the potential therapeutic value of PARP inhibitors in this devastating complication of diab

155 vels of PAR, which predicted the response to PARP inhibitors in vitro and in vivo more accurately tha

156 tinum drugs and poly(ADP-ribose) polymerase (PARP) inhibitors in clinical trials.

157 oncept by using poly(ADP-ribose) polymerase (PARP) inhibitors in patients with germline BRCA1 or BRCA

158 A phase I trial of ABT-888 (veliparib), a PARP inhibitor, in combination with topotecan, a topoiso

159 nases whose silencing strongly sensitised to PARP inhibitor, including cyclin-dependent kinase 5 (CDK

160 These data suggest that low-potency PARP inhibitors increase insulin biosynthesis, in part,

161 , orally active poly(ADP-ribose) polymerase (PARP) inhibitor, induced synthetic lethality in BRCA-def

162 dependency to PARP1, becoming susceptible to PARP inhibitor-induced apoptosis.

163 ogether, we suggest that ATM is activated by PARP inhibitor-induced collapsed replication forks and m

164 Furthermore, PARP inhibitor-induced HRR is abolished in ATM, but not

165 suggesting that mitotic progression promotes PARP-inhibitor-induced cell death.

166 otic bypass through EMI1 depletion abrogates PARP-inhibitor-induced cytotoxicity.

167 PARP-inhibitor-induced multinucleated cells fail clonoge

168 of BRCA1-mediated HR, the administration of PARP inhibitors induces synthetic lethality of tumour ce

169 l lines with a combination of DNA ligase and PARP inhibitors inhibited ALT NHEJ and selectively decre

170 ed the effects of two structurally unrelated PARP inhibitors (INO-1001 and PJ-34) on the development

171 This lethality of the PARP inhibitor is dependent on apurinic/apyrimidinic (AP

172 The development of PARP inhibitors is being pursued as a therapeutic approa

173 Treatment with PARP inhibitors is likely to be highly tumour specific,

174 ometrial cancers, the therapeutic utility of PARP inhibitors is limited in this disease.

175 for the sensitivity of HR-defective cells to PARP inhibitors is related to the hyperactivated PARP1 i

176 tential when a poly (ADP-ribose) polymerase (PARP) inhibitor is given for the treatment of advanced T

177 e, leading to the development of therapeutic PARP inhibitors, many of which are currently in clinical

178 Our findings indicate that PARP inhibitors may be a novel therapeutic strategy for

179 d FdUrd and suggest that combining FdUrd and PARP inhibitors may be an innovative therapeutic strateg

180 for BRCA1 or BRCA2 deficiency suggests that PARP inhibitors may be particularly useful for the treat

181 at treatment with a combination of c-Met and PARP inhibitors may benefit patients whose tumors show h

182 tion of mechanisms of cellular resistance to PARP inhibitors may provide indications as to how these

183 ribe recent advances in our understanding of PARP inhibitor mechanism of action, and discuss current

184 some of the principles learned in developing PARP inhibitors might also drive the development of addi

185 Recent evidence has suggested that PARP inhibitors might be active as single agents in cert

186 ch might restrict the therapeutic utility of PARP inhibitor monotherapy.

187 e are still unanswered questions surrounding PARP inhibitors, namely the levels of specificity and po

188 The low-potency PARP inhibitors nicotinamide, 3-aminobenzamide, or PD128

189 Among 10 widely used PARP inhibitors, none affected DSB repair, although an i

190 1 and BRCA2 mutations being treated with the PARP inhibitor olaparib (AZD2281, KU-0059436; KuDOS/Astr

191 dometrial cancer cells are not responsive to PARP inhibitor Olaparib alone, but instead show superior

192 estingly, EGFR-mutant cells treated with the PARP inhibitor olaparib also displayed decreased FAN1 fo

193 mors, exhibited increased sensitivity to the PARP inhibitor olaparib as compared to MPCs transformed

194 tations exhibited favorable responses to the PARP inhibitor olaparib compared with patients without B

195 Finally, we demonstrated that PARP inhibitor olaparib did not significantly alter the

196 Treatment with the PARP inhibitor olaparib in patients whose prostate cance

197 pporting this possibility, we found that the PARP inhibitor olaparib or ATR inhibitors reduced the vi

198 ian cancer, maintenance monotherapy with the PARP inhibitor olaparib significantly improves progressi

199 Maintenance monotherapy with the PARP inhibitor olaparib significantly prolonged progress

200 r suberoylanilide hydroxamic acid (SAHA) and PARP inhibitor olaparib, and identified one pair of cell

201 y, augmented the effects of cisplatin or the PARP inhibitor olaparib, and improved the response of pl

202 sphomimetic Mre11 were more sensitive to the PARP inhibitor olaparib, compared with those expressing

203 partly resensitize sarcomatoid tumors to the PARP inhibitor olaparib, docetaxel, and doxorubicin.

204 the response of BRCA1-deficient MBCs to the PARP inhibitor olaparib.

205 cient cells and tumors were sensitive to the PARP inhibitor olaparib.

206 served that the poly(ADP-ribose) polymerase (PARP) inhibitor olaparib synergizes with GLS1 inhibitors

207 tly sensitive to poly-ADP-ribose polymerase (PARP) inhibitors olaparib and BMN673.

208 served that the poly(ADP-ribose) polymerase (PARP) inhibitors olaparib and veliparib sensitize the my

209 itizes ovarian cancer cells to cisplatin and PARP inhibitor (olaparib) while overexpression of USP13

210 One PARP inhibitor, olaparib (Lynparza, AstraZeneca), was re

211 tive to agents that cause DSBs including the PARP inhibitor, olaparib.

212 -EGFR monoclonal antibody, chemotherapy, and PARP inhibitors on cell death and the survival of breast

213 en the 2 cell types, while the presence of a PARP inhibitor or use of PARPKO BMDCs in the incubation

214 ruption of PARP, itself, either via chemical PARP inhibitors or siRNAs targeted to PARP-1, can inhibi

215 butoxy]-1(2H)-isoquinolinone, an established PARP inhibitor, or by 100 nM minocycline.

216 nd after treatment with olaparib (n = 14), a PARP inhibitor, or iniparib (n = 11), which has no PARP

217 have clinically benefitted from therapy with PARP inhibitor (PARPi) or platinum compounds, but acquir

218 Platinum and PARP inhibitor (PARPi) sensitivity commonly coexist in e

219 correlated with in vitro sensitivity to the PARP inhibitor (PARPi), rucaparib.

220 reader on PARP function, the development of PARP inhibitors (PARPi) and the evidence for targeting P

221 PARP inhibitors (PARPi) benefit only a fraction of breas

222 PARP inhibitors (PARPi), a cancer therapy targeting poly

223 es the relative sensitivity of PDAC cells to PARP inhibitors (PARPi).

224 air machinery, which makes them sensitive to PARP inhibitors (PARPi).

225 Poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi) olaparib has been approved for t

226 this pathway by Poly(ADP-ribose) polymerase (PARP) inhibitors (PARPi) is toxic to cells with defects

227 PARP inhibitors (PARPis) are being used in patients with

228 To enhance the clinical response to PARP inhibitors (PARPis), understanding the mechanisms u

229 , impairs DDR and sensitizes MLL leukemia to PARP inhibitors (PARPis).

230 Poly-(ADP-ribose) polymerase (PARP) inhibitors (PARPis) selectively kill BRCA1/2-defic

231 s with and intradermal in vivo injections of PARP inhibitor, PJ-34, caused WT-level cyclobutane pyrim

232 The treatment group received the PARP inhibitor PJ34 (PJ34) over a 24-hour period; the un

233 nd liver, as cotreatment with dioxin and the PARP inhibitor PJ34 increased NAD(+) levels and prevente

234 blocking PARP activity with the competitive PARP inhibitors PJ34 or INO-1001.

235 PJ34 and UPF1069 are broad PARP inhibitors; PJ34 inserts a flexible moiety into hyd

236 Our biochemical and structural analysis of PARP inhibitor potencies establishes a molecular basis f

237 gous recombination, are acutely sensitive to PARP inhibitors, presumably because resultant collapsed

238 ivation of Tet activity because the use of a Parp inhibitor prevented demethylation of specific loci

239 Both PARP inhibitors reduced diabetes-induced retinal oxidati

240 PARP inhibitors represent a novel therapeutic strategy t

241 Poly(ADP-Ribose) (PAR) polymerase (PARP) inhibitors represent a promising class of novel an

242 , RADX inactivation confers chemotherapy and PARP inhibitor resistance to cancer cells with reduced B

243 ficient cells, leading to HR restoration and PARP inhibitor resistance, which is reversed by ATM kina

244 Here, we report that PARP inhibitor-resistant BRCA2-mutant cells revert back

245 We derived PARP-inhibitor-resistant (PIR) clones from the human CAP

246 PARP-1-binding site or upon treatment with a PARP inhibitor, respectively.

247 uman insulin promoter mapped the low-potency PARP inhibitor response to the C1 element, which serves

248 A repair and suggest PPP2R2A as a marker for PARP inhibitor responses in clinic.

249 Association with poly-ADP ribose polymerase (PARP) inhibitor responsiveness and with radiation-induce

250 Low-potency PARP inhibitors restored MafA mRNA and protein levels, b

251 , oxaliplatin, cisplatin, carboplatin, and a PARP inhibitor) results in HuR's translocation from the

252 ed a relative increase in sensitivity to the PARP inhibitor rucaparib and slower orthotopic tumor gro

253 iveness of radiation in combination with the PARP inhibitor, rucaparib in PCa cells.

254 of a BRCT domain mutant BRCA1 protein under PARP inhibitor selection pressure.

255 as well as the molecular mechanism by which PARP inhibitors selectively kill tumor cells with BRCA m

256 gly, BCL2 expression reduced the survival of PARP inhibitor-sensitive breast cancer and lung cancer c

257 ized that ectopic BCL2 expression would kill PARP inhibitor-sensitive cells.

258 s with these revertant BRCA2 alleles rescued PARP inhibitor sensitivity and HR deficiency.

259 insight into the mechanisms of cisplatin and PARP inhibitor sensitivity of EGFR-mutant cells, yieldin

260 erest in finding alternative determinants of PARP inhibitor sensitivity.

261 ing the RAD51D-XRCC2 interaction and confers PARP inhibitor sensitivity.

262 patient-derived tumor specimens, and between PARP-inhibitor sensitivity and resistance in four out of

263 in RAD51D are sensitive to treatment with a PARP inhibitor, suggesting a possible therapeutic approa

264 f sensitivity to these drugs, we performed a PARP-inhibitor synthetic lethal short interfering RNA (s

265 PARP inhibitors target homologous recombination (HR)-def

266 Olaparib is a potent, oral PARP inhibitor that is well tolerated, with antitumor ac

267 say can be used to determine IC50 values for PARP inhibitors that have a range of inhibitory properti

268 Clinical development of PARP inhibitors that target DNA repair defects in cancer

269 , orally active poly(ADP-ribose) polymerase (PARP) inhibitor that induces synthetic lethality in homo

270 predicting sensitivity to platinum salts and PARP inhibitors, the data regarding somatic mutation for

271 ant to the proposed therapeutic mechanism of PARP inhibitors, the physical makeup and dynamics of thi

272 lity allele and supports the use of targeted PARP-inhibitor therapies in ovarian cancer patients carr

273 strategy using poly(ADP)-ribose polymerase (PARP) inhibitor therapy in BRCA1/2 mutation carriers in

274 enzymatic activity and reduces binding to a PARP inhibitor, thereby rendering cancer cells resistant

275 usible strategy for expanding the utility of PARP inhibitors to BRCA-proficient cancers.

276 plausible approach to expand the utility of PARP inhibitors to endometrioid endometrial cancers in a

277 In this study, we show that PARP inhibitors trap the PARP1 and PARP2 enzymes at dama

278 eated cells are found in vivo in remnants of PARP inhibitor-treated Brca2(-/-);p53(-/-) and Brca1(-/-

279 Here, we show that PARP inhibitor treatment induces phosphorylation of DNA-

280 point at combination therapies to potentiate PARP inhibitor treatment of HR-deficient tumours.

281 Further analysis demonstrated that PARP inhibitor treatment results in activation of the FA

282 gets whose ADP-ribosylation was sensitive to PARP inhibitor treatment.

283 Here, we show that PARP inhibitors trigger gamma-H2AX and RAD51 foci format

284 h cisplatin, topotecan, gemcitabine, and the PARP inhibitor veliparib (ABT-888), four agents with cli

285 s to probe cell line-specific effects of the PARP inhibitor Veliparib and radiation on metabolism in

286 n this study we evaluated the ability of the PARP inhibitor veliparib to enhance the cytotoxicity of

287 atin and to the poly(ADP-ribose) polymerase (PARP) inhibitor veliparib (ABT-888).

288 Increased MafA expression by low-potency PARP inhibitors was independent of increased MafA protei

289 king agents and poly(ADP-ribose) polymerase (PARP) inhibitors, we sought to investigate the response

290 Poly (ADP-ribose) polymerase (PARP) inhibitors were found to be "synthetic lethal" in

291 her low-potency poly(ADP-ribose) polymerase (PARP) inhibitors were thus tested for their ability to r

292 ify HR-defective cells that are sensitive to PARP inhibitors, which may be potential biomarkers.

293 Thus, poly(ADP-ribose) polymerase (PARP) inhibitors, which disrupt BER, markedly sensitize

294 nical trials of poly(ADP-ribose) polymerase (PARP) inhibitors, which require an HR defect for efficac

295 he next steps necessary to determine whether PARP inhibitors will finally make the difference in trea

296 However, developing a new type PARP inhibitor with distinctive skeleton is alternativel

297 c amine-containing benzimidazole carboxamide PARP inhibitors with a methyl-substituted quaternary cen

298 a synergistic drug combination of allosteric PARP inhibitors with DNA-damaging agents in genomically

299 However, the mechanism of action of PARP inhibitors with regard to their effects in cancer c

300 ole carboxamide poly(ADP-ribose) polymerase (PARP) inhibitors with excellent PARP enzyme potency as w