ライフサイエンスコーパス: PARP Inhibitor

1 repared and characterized a very long-acting PARP inhibitor.

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

3 most likely to respond therapeutically to a PARP inhibitor.

4 sitizes tumor cell to chemically synthesized PARP inhibitors.

5 HRR-proficient epithelial ovarian cancers to PARP inhibitors.

6 ed by treatment with DNA-damaging agents and PARP inhibitors.

7 to DNA-damaging agents such as platinum and PARP inhibitors.

8 patients that are more likely to respond to PARP inhibitors.

9 an NAD(+) derivative, are more sensitive to PARP inhibitors.

10 g synergy with DNA-damaging chemotherapy and PARP inhibitors.

11 and confer resistance to platinum salts and PARP inhibitors.

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

13 PN cells to synthetic lethality triggered by PARP inhibitors.

14 xic sensitivity of cell lines evaluated with PARP inhibitors.

15 e maintenance and regulating the efficacy of PARP inhibitors.

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

17 ithelial cells and to enhance sensitivity to PARP inhibitors.

18 has important implications for the design of PARP inhibitors.

19 may benefit from either platinum therapy or PARP inhibitors.

20 at may be useful therapeutic alternatives to PARP inhibitors.

21 fficient for patients to derive benefit from PARP inhibitors.

22 mbination may also have predictive value for PARP inhibitors.

23 biomarkers for breast cancer sensitivity to PARP inhibitors.

24 honates as potential combination therapy for PARP inhibitors.

25 py, which may expand the clinical utility of PARP inhibitors.

26 tant determinant of the response to clinical PARP inhibitors.

27 nature analysis, that may be targetable with PARP inhibitors.

28 ic response to poly (ADP-Ribose) polymerase (PARP) inhibitor.

29 es the resistance of BRCA-deficient cells to PARP-inhibitors.

30 ulnerability to poly(ADP-ribose) polymerase (PARP) inhibitors.

31 herapies such as poly-ADP ribose polymerase (PARP) inhibitors.

32 sensitivity to poly(ADP-ribose) polymerase (PARP) inhibitors.

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

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

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

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

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

38 a radiolabeled poly(ADP-ribose) polymerase (PARP) inhibitor, (125)I-KX1, we delivered an Auger emitt

39 ynthesis of the poly(ADP-ribose) polymerase (PARP) inhibitor [(18)F]olaparib.

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

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

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

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

44 We demonstrated that two PARP inhibitors (ABT-888 and olaparib) make SNP carrier

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

46 strategy for enhancing the effectiveness of PARP inhibitors against TNBC.

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

48 preclinical efficacy of combination olaparib PARP inhibitor and temozolomide DNA-damaging agent as an

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

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

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

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

53 tizes triple-negative breast cancer cells to PARP inhibitors and DNA-damaging chemotherapeutics by re

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

55 ribe can explain mechanisms of resistance to PARP inhibitors and will aid the development of better i

56 r resistance to poly(ADP-ribose) polymerase (PARP) inhibitors and other therapeutics and for the deve

57 re sensitive to poly(ADP-ribose) polymerase (PARP) inhibitors and platinum agents owing to deficiency

58 are sensitive to poly(ADP)ribose polymerase (PARP) inhibitors and that the processing of spontaneous

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

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

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

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

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

64 PARP inhibitors are approved for treatment of cancers wi

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

66 cause of their specific mechanism of action, PARP inhibitors are not completely benign and overall sh

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

68 PARP inhibitors are promising therapeutic agents that sh

69 adenosine 5'-diphosphate-ribose) polymerase (PARP) inhibitors are a class of anticancer drugs that bl

70 Poly(ADP-ribose) polymerase (PARP) inhibitors are increasingly being studied as cance

71 filing is recommended for the development of PARP inhibitors as PARP-kinase polypharmacology could po

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

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

74 and maintenance poly(ADP-ribose) polymerase (PARP) inhibitors both significantly improve efficacy ver

75 compares all toxicities associated with each PARP inhibitor, both in monotherapy and in novel combina

76 s similar binding sites with PARP with other PARP inhibitors, but pamiparib is not a P-gp substrate a

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

78 ly(adenosine diphosphate ribose) polymerase (PARP) inhibitor called (125)I-KX1 to deliver Auger radia

79 AR conjugation (PARylation): PAR polymerase (PARP) inhibitors can modulate the formation and dynamics

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

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

82 cancer cell lines, and a far richer array of PARP inhibitor combination therapies for BRCA1-deficient

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

84 Here, we found that olaparib, a FDA-approved PARP inhibitor, could enhance the cytotoxicity in HCC ce

85 nes exhibit sensitivity to topoisomerase and PARP inhibitors, defective sister chromatid cohesion and

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

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

88 rtant to Ad infection since treatment with a PARP inhibitor enhances replication efficiency.

89 sensitivity to poly(ADP-ribose) polymerase (PARP) inhibitors, especially when combined with radiothe

90 ummarised with a focus on median duration of PARP inhibitor exposure, median latency period between f

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

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

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

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

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

96 stance during cancer therapy and repurposing PARP inhibitors for the treatment of non-oncological dis

97 o far led to the regulatory approval of four PARP inhibitors for the treatment of several types of ca

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

99 Tumors resistant to PARP inhibitors frequently show signs of replication str

100 ten non-placebo RCTs), with 5693 patients in PARP inhibitor groups and 3406 patients in control group

101 syndrome and acute myeloid leukaemia across PARP inhibitor groups was 0.73% (95% CI 0.50-1.07; I(2)=

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

103 defect after BRCA2, but their sensitivity to PARP inhibitors has been questioned by recent clinical l

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

105 We demonstrate that all four PARP inhibitors have a unique polypharmacological profil

106 he treatment of several types of cancer, and PARP inhibitors have also shown therapeutic potential in

107 Four PARP inhibitors have been approved by the FDA as cancer

108 complicating this situation, three different PARP inhibitors have been approved by the US Food and Dr

109 e best-known element of the DDR, and several PARP inhibitors have been licensed.

110 PARP inhibitors have been proven clinically efficacious

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

112 While PARP inhibitors have been tested in clinical trials and

113 failures can lead to human disease, and how PARP inhibitors have emerged as a novel clinical therapy

114 his effect of PARP in the tumor cell itself, PARP inhibitors have emerged as new therapeutic tools bo

115 role in DNA damage repair and small molecule PARP inhibitors have emerged as potent anticancer drugs.

116 PARP inhibitors have shown remarkable efficacy in the cl

117 Efforts to identify and evaluate potent PARP inhibitors have so far led to the regulatory approv

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

119 rapies such as poly (ADP-ribose) polymerase (PARP) inhibitors have emerged as one of the most excitin

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

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

122 Poly(ADP-ribose) polymerase (PARP) inhibitors have shown efficacy and acceptable safe

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

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

125 t the most potently inhibited off-targets of PARP inhibitors identified to date and should be investi

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

127 Furthermore, chemical PARP inhibitors improve axon regeneration when administe

128 4-003319-12), we investigate the activity of PARP inhibitors in 43 patients with untreated TNBC.

129 etween AR-Vs and PARP, advocating the use of PARP inhibitors in AR-V positive PC.

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

131 itizes CARM1-high, but not CARM-low, EOCs to PARP inhibitors in both orthotopic and patient-derived x

132 onses; therefore, this enzyme is targeted by PARP inhibitors in cancer therapy.

133 al biomarker for therapeutic treatment using PARP inhibitors in cancers.

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

135 iciency and the potential therapeutic use of PARP inhibitors in DLBCL and T-ALL.

136 ases for the efficacy of mTORC1, CDK4/6, and PARP inhibitors in metastatic breast cancer.

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

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

139 dicate the utility of combining platinum and PARP inhibitors in this patient population.

140 RDMT1 in cancer cells confers sensitivity to PARP inhibitors in vitro and in vivo.

141 ly(adenosine diphosphate-ribose) polymerase (PARP) inhibitor in a CARM1-dependent manner.

142 inhibitors and poly (ADP-ribose) polymerase (PARP) inhibitors in a variety of solid tumours.

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

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

145 PARP inhibitors increased the risk of myelodysplastic sy

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

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

148 PARP-inhibitor-induced multinucleated cells fail clonoge

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

150 ctive agents targeting DNA repair, including PARP inhibitors; inhibitors of the DNA damage kinases at

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

152 haps the most advantageous characteristic of PARP inhibitors is their mechanism of action, which targ

153 um-based chemotherapy with a plan to receive PARP inhibitor maintenance.

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

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

156 However, resistance to PARP inhibitors may preexist or evolve during treatment

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

158 ort that loss of ALC1 confers sensitivity to PARP inhibitors, methyl-methanesulfonate, and uracil mis

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

160 hat targeting R-loops with topoisomerase and PARP inhibitors might be an effective treatment strategy

161 Although the excitement surrounding PARP inhibitors might certainly be warranted, a thorough

162 ollection nine BRCAm patients had received a PARP inhibitor off-trial, three had entered a PARP inhib

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

164 CL1 upregulation but remain sensitive to the PARP inhibitor olaparib and the pan-BCL inhibitor obatoc

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

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

167 identify the recommended phase 2 dose of the PARP inhibitor olaparib in combination with the PI3K inh

168 ed, open-label, phase 3 trial evaluating the PARP inhibitor olaparib in men with metastatic castratio

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

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

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

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

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

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

175 strate that AZD7648, in combination with the PARP inhibitor olaparib, increases genomic instability,

176 mutant and wild-type BRCA1 TNBC cells to the PARP inhibitor olaparib.

177 of the Food and Drug Administration-approved PARP inhibitor olaparib.

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

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

180 augments the antiproliferative effect of the PARP inhibitor olaparib.

181 thousands of endogenous proteins to clinical PARP inhibitors Olaparib and Rucaparib.

182 icity with the poly (ADP-ribose) polymerase (PARP) inhibitor olaparib against TNBC cells.

183 The poly (ADP-ribose) polymerase (PARP) inhibitor olaparib is FDA approved for the treatme

184 potecan or the poly-(ADP-ribose) polymerase (PARP) inhibitor olaparib reflects delayed engagement of

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

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

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

188 Poly (ADP-ribose) polymerase (PARP) inhibitors (olaparib and talazoparib) are preferab

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

190 lnerable to the poly(ADP-ribose) polymerase (PARP) inhibitor, olaparib, and prolonged survival in tum

191 dings warrant careful examination of current PARP inhibitors on bone metastasis and bone loss, and su

192 ct patients for poly(ADP-ribose) polymerase (PARP) inhibitor or platinum chemotherapy, and mismatch r

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

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

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

196 block DNA end resection at DSBs and increase PARP inhibitor (PARPi) sensitivity.

197 g agent temozolomide in combination with the PARP inhibitor (PARPi) talazoparib.

198 PARP inhibitor (PARPi) therapy targets BRCA1/2 mutant tu

199 BRCA1 mutant carcinomas are sensitive to PARP inhibitor (PARPi) therapy; however, resistance aris

200 As most currently approved PARP inhibitors (PARPi) are MDR1 substrates, prior chemo

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

202 Clinical PARP inhibitors (PARPi) extend the lifetime of damage-in

203 PARP inhibitors (PARPi) have shown remarkable therapeuti

204 Despite the high initial response rates to PARP inhibitors (PARPi) in BRCA-mutated epithelial ovari

205 One example is the use of PARP inhibitors (PARPi) in oncology patients with BRCA m

206 Acquired resistance to PARP inhibitors (PARPi) is a major challenge for the cli

207 PARP inhibitors (PARPi) prevent cancer cell growth by in

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

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

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

211 ires resistance to platinum chemotherapy and PARP inhibitors (PARPi).

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

213 Olaparib, a poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi), is approved for the treatment o

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

215 PARP inhibitors (PARPis) are used clinically to treat BR

216 PARP inhibitors (PARPis) have clinical efficacy in BRCA-

217 Clinical activity of PARP inhibitors (PARPis) in BRCA1/2 mutant cancers valid

218 However, resistance to PARP inhibitors (PARPis) is common.

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

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

221 otoxic effects, poly(ADP ribose) polymerase (PARP) inhibitors (PARPis) exhibit antitumor immunity tha

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

223 sensitivity to poly (ADP-ribose) polymerase (PARP) inhibitors (PARPis), but the role for PARPis in BR

224 nt response to poly (ADP-ribose) polymerase (PARP) inhibitors; patients with ovarian cancer whom we f

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

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

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

228 al motif of new poly(ADP-ribose) polymerase (PARP) inhibitors, playing a useful role in multiple phar

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

230 It may also explain the mechanism by which PARP inhibitor regulates early DNA damage repair.

231 alysis, and to describe clinical features of PARP inhibitor-related myelodysplastic syndrome and acut

232 allenges in the field, such as counteracting PARP inhibitor resistance during cancer therapy and repu

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

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

235 summarize what is known about mechanisms of PARP inhibitor resistance.

236 ells, promotes REV7 inactivation, and causes PARP inhibitor resistance.

237 on to DSBs, and poly(ADP-ribose) polymerase (PARP) inhibitor resistance.

238 sponse despite being platinum refractory and PARP inhibitor resistant.

239 chronic treatment of BRCA1-mutant cells with PARP inhibitors, resistant clones can arise via several

240 In PARP inhibitor-resistant A172 glioblastoma cells, our PA

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

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

243 ral TLZ and would be useful for treatment of PARP inhibitor-sensitive cancers in which oral medicatio

244 1140G [c.3418T>C], stood out with pronounced PARP inhibitor sensitivity and cytoplasmic accumulation

245 Because PARG and PARP inhibitor sensitivity are mutually exclusive, our o

246 decreased USP15-BARD1 interaction, increases PARP inhibitor sensitivity in cancer cells.

247 ons in DDR genes beyond BRCA1/2 in mediating PARP inhibitor sensitivity is poorly understood.

248 Manipulating NuMA expression alters PARP inhibitor sensitivity of BRCA1-null cells, end-join

249 mologous recombination DNA repair pathway or PARP inhibitor sensitivity, first in a pan-cancer cohort

250 e reasonably good at predicting platinum and PARP inhibitor sensitivity.

251 lts in increased nascent DNA degradation and PARP inhibitor sensitivity.

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

253 Hence, targeting ALC1 alone or as a PARP inhibitor sensitizer could be employed to augment e

254 ys a significant up-regulation of PARP1, and PARP inhibitors significantly delay tumor growth and met

255 ed on the 18 placebo RCTs (n=7307 patients), PARP inhibitors significantly increased the risk of myel

256 Importantly, we find that treatment with PARP inhibitors stimulates the interferon response in ce

257 ors have therapeutic potential to complement PARP inhibitor strategies in the treatment of ovarian ca

258 Furthermore, chemotherapy and PARP inhibitors synergize to inhibit the growth of LMO2-

259 tic prostate cancer patient treated with the PARP inhibitor talazoparib exhibited similar CSC marker

260 le injection of a long-acting prodrug of the PARP inhibitor talazoparib in murine xenografts provides

261 mall molecule Poly(ADP-ribose) polymerase-1 (PARP) inhibitor, talazoparib led to increased DNA double

262 we demonstrated that PARPi-FL, a fluorescent PARP inhibitor targeting the enzyme PARP1/2, can delinea

263 ur study identifies NADP(+) as an endogenous PARP inhibitor that may have implications in cancer trea

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

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

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

267 tes with response to platinum (P < .001) and PARP inhibitor therapy (P < .001) in vitro and in vivo.

268 andomised controlled trials (RCTs) comparing PARP inhibitor therapy versus control treatments (placeb

269 drome and acute myeloid leukaemia related to PARP inhibitor therapy were extracted on May 3, 2020, an

270 nd acute myeloid leukaemia (n=79) related to PARP inhibitor therapy were extracted.

271 re likely to benefit from ATR inhibitor than PARP inhibitor therapy.

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

273 olymerase 1 (PARP1)-DNA complexes trapped by PARP inhibitors, thereby promoting cell survival after d

274 ying a combined therapy of GLS inhibitor and PARP inhibitor to treat chemoresistant ovarian cancers,

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

276 enges to extend the therapeutic potential of PARP inhibitors to other cancer types is the absence of

277 s, ultimately causing mitotic catastrophe in PARP inhibitor treated HR-proficient cells.

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

279 However, to date, PARP inhibitor treatment has been restricted to patients

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

281 PARP inhibitor treatment suppressed the immediate histon

282 ombination repair and therefore sensitive to PARP inhibitor treatment.

283 in cancer cells and thus sensitize cells to PARP inhibitor treatment.See related articles by Luo et

284 e important survival pathways in response to PARP-inhibitor treatment.

285 ARP inhibitor off-trial, three had entered a PARP inhibitor trial and 5 were receiving platinum-based

286 Data are insufficient to recommend PARP inhibitor use in the early setting or in moderate-p

287 ersensitive to poly (ADP-ribose) polymerase (PARP) inhibitors used to treat BRCA1/2-deficient cancers

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

289 drome and acute myeloid leukaemia related to PARP inhibitors, via a systematic review and safety meta

290 ian latency period since first exposure to a PARP inhibitor was 17.8 months (8.4-29.2; n=58).

291 t with bevacizumab or first-line maintenance PARP inhibitors was permitted.

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

293 ls lack RAD51 foci and are hypersensitive to PARP inhibitor, whereas forced targeting of PALB2 to DNA

294 nces clinical management, such as the use of PARP inhibitors, which have demonstrated a progression-f

295 ore vulnerable to ATR inhibition rather than PARP inhibitors, which is a testable hypothesis for clin

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

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

298 ancer types and may be overcome by combining PARP inhibitors with other therapies, such as immune che

299 in HR repair and suggest that combination of PARP inhibitors with radiotherapy could be an effective

300 combination of poly (ADP-ribose) polymerase (PARP) inhibitors with drugs that inhibit the homologous