ライフサイエンスコーパス: ovarian cancer

1 in acquired resistance to platinum drugs in ovarian cancer.

2 by mutated TP53, a gene commonly altered in ovarian cancer.

3 atinum-sensitive, relapsed high-grade serous ovarian cancer.

4 es in patients with suspected advanced-stage ovarian cancer.

5 M expression and reduced overall survival in ovarian cancer.

6 s (CAFs) contribute to the poor prognosis of ovarian cancer.

7 nvasive end-of-life care among patients with ovarian cancer.

8 intrabursal mouse xenograft models of human ovarian cancer.

9 logical function of IL-6R mRNA expression in ovarian cancer.

10 R) DNA repair genes are linked to breast and ovarian cancer.

11 inical trials in patients with leukaemia and ovarian cancer.

12 des a therapeutic strategy for highly lethal ovarian cancer.

13 urvival and chemoresistance in patients with ovarian cancer.

14 r use in liposomal form for the treatment of ovarian cancer.

15 nts with high grade but not low grade serous ovarian cancer.

16 ted with 10 kilobase tandem duplications in ovarian cancer.

17 n of CS-E, which is a possible biomarker for ovarian cancer.

18 n tissue phantoms and in an in vivo model of ovarian cancer.

19 le-appearing cysts were given a diagnosis of ovarian cancer.

20 CA2 severely increase the risk of breast and ovarian cancer.

21 variant carriers have an increased risk for ovarian cancer.

22 mation and development of drug resistance in ovarian cancer.

23 detect sentinel nodes (SNs) in patients with ovarian cancer.

24 tly is the best serum-based tumor marker for ovarian cancer.

25 of metastatic hepatic involvement in serous ovarian cancer.

26 e Ciota (PKCiota) is an oncogene in lung and ovarian cancer.

27 ties in end-of-life care among patients with ovarian cancer.

28 with FRalpha-positive and platinum-resistant ovarian cancer.

29 hich indicates its therapeutic potential for ovarian cancer.

30 years) or a family history of breast and/or ovarian cancer.

31 ve been identified as potent EMT inducers in ovarian cancer.

32 that UBR5 can confer cisplatin resistance in ovarian cancer.

33 n patients with platinum-sensitive recurrent ovarian cancer.

34 underlying platinum and taxane resistance in ovarian cancer.

35 rring, growth-promoting mutational events in ovarian cancer.

36 a cell-line xenograft model of disseminated ovarian cancer.

37 and human myeloid dendritic cells (TIDC) in ovarian cancer.

38 nt and treatment of patients with breast and ovarian cancer.

39 target genes for future treatment efforts in ovarian cancer.

40 berrations responsible for poor prognosis in ovarian cancer.

41 LPP enhances the efficacy of chemotherapy in ovarian cancer.

42 trend = 0.01) were inversely associated with ovarian cancer.

43 eatic adenocarcinoma and advanced epithelial ovarian cancer.

44 sible role of tumoral expression of IL-6R in ovarian cancer.

45 reclinical models of advanced pancreatic and ovarian cancer.

46 serum biomarker and a therapeutic target for ovarian cancer.

47 as a novel therapeutic target for resistant ovarian cancer.

48 d may provide a new therapeutic strategy for ovarian cancer.

49 olvement of this gene in the commencement of ovarian cancers.

50 ated in many colorectal, hepatocellular, and ovarian cancers.

51 ognosis and treatment response in breast and ovarian cancers.

52 orse overall survival in breast, uterine and ovarian cancers.

53 onsortium (OCAC), including 9,162 women with ovarian cancers, 2,354 women with borderline tumors, and

54 curacy for the screening pelvic examination: ovarian cancer (4 studies; n = 26432), bacterial vaginos

55 In a xenograft model of human ovarian cancer, a nanoparticle-mediated siRNA strategy t

56 ation between PID and the risk of epithelial ovarian cancer according to tumor behavior and histotype

57 High-grade serous (HGS) ovarian cancer accounts for 90% of all ovarian cancer-re

58 In an established mouse xenograft model of ovarian cancer, adoptive transfer of NK cells conditione

59 %, 1.0%) of 2763 patients were found to have ovarian cancer after an average follow-up of 5.1 years +

60 nificant prognostic value in both breast and ovarian cancers after considering established clinical v

61 healthy women with advanced-stage epithelial ovarian cancer aged 70 years or younger.

62 125 (CA-125), interpreted using the risk of ovarian cancer algorithm (ROCA), and transvaginal sonogr

63 rescent dyes to mice bearing intraperitoneal ovarian cancer allowed visualization of tumor-associated

64 38 years; IQR, 31-47 years) eligible for the ovarian cancer analysis, and 2213 women (median age, 47

65 51.4%) had a mother or sister with breast or ovarian cancer and 54 patients (48.6%) did not.

66 d agents currently used to treat BRCA-mutant ovarian cancer and are in clinical trials for other canc

67 llected from patients with colon, breast, or ovarian cancer and cell lines harboring specific oncogen

68 fectiveness of HDAC inhibitors when treating ovarian cancer and other solid tumors characterized by i

69 little is known about the effects of DHM on ovarian cancer and the underlying mechanisms.

70 erved in gastrointestinal, lung, breast, and ovarian cancer and this could decrease the threshold req

71 tromal and tumour compartments of aggressive ovarian cancers and its levels correlate with poor clini

72 We used the keywords "ovarian cancer" and searched through GEO database and fi

73 were diagnosed with breast cancer, 109 with ovarian cancer, and 245 with contralateral breast cancer

74 with a focus on melanoma, and pancreatic and ovarian cancer, and discuss how scientific advances may

75 K2) is highly expressed in high-grade serous ovarian cancer, and we investigated its role in Akt acti

76 al differences between serous and non-serous ovarian cancers, and further distinguish different non-s

77 f benign sources has unveiled a multitude of ovarian cancer antigens (MUC16, MSLN, LGALS1, IDO1, KLK1

78 Cancer-specific glycans of ovarian cancer are promising epitopes for targeting with

79 Advanced-stage epithelial ovarian cancers are amongst the most difficult to treat

80 helicase is linked to hereditary breast and ovarian cancers as well as bone marrow failure disorder

81 studies have reported decreased incidence of ovarian cancer associated with regular intake of NSAIDs,

82 s, conducted between 1989 and 2009, from the Ovarian Cancer Association Consortium (OCAC), including

83 Patients with known ovarian cysts or ovarian cancer at time of the index CT examination were

84 neal xenografts and prolongs the survival of ovarian cancer-bearing mice.

85 aparib has durable benefit for patients with ovarian cancer beyond germline BRCA1/2 carriers.

86 was detected in 43 (68.3%) of 63 women with ovarian cancer but in none of 50 healthy controls.

87 The study was conducted among 415 ovarian cancer cases and 629 age- and site-matched contr

88 In vitro treatment of breast and ovarian cancer cell cultures in aqueous media by tamoxif

89 2133 (IC50 > 25 muM) inhibited the growth of ovarian cancer cell cultures.

90 Suppressing KDM4B inhibits ovarian cancer cell invasion, migration and spheroid for

91 Following infection of a human ovarian cancer cell line (OVCAR3) with a recombinant low

92 ne fusions missed by other algorithms in the ovarian cancer cell line OVCAR3.

93 cell death and DNA damage was studied in two ovarian cancer cell lines (OVCAR3 and A2780), normal ham

94 ow that MICU1 is overexpressed in a panel of ovarian cancer cell lines and that MICU1 overexpression

95 The bioenergetics phenotype of ovarian cancer cell lines correlated with functional phe

96 MGCR), was found to be over-expressed in all ovarian cancer cell lines examined and upregulated by mu

97 portantly, we found that cisplatin-resistant ovarian cancer cell lines exhibit lower levels of MOAP-1

98 spheroids compared to monolayer cultures of ovarian cancer cell lines or primary cells.

99 ing of 13 established and 12 patient derived ovarian cancer cell lines revealed significant bioenerge

100 y against cisplatin-resistant A2780Cis human ovarian cancer cells (IC50 74 muM, blue light) with a ph

101 tified Nectin-4 shedding from the surface of ovarian cancer cells after stimulation with lysophosphat

102 uld effectively inhibit the proliferation of ovarian cancer cells and induce cell apoptosis.

103 rate that metastasis-associated behaviors of ovarian cancer cells and MCAs are influenced by cellular

104 d platinum-sensitive and platinum- resistant ovarian cancer cells and ovarian cancer stem cells and (

105 9), which is upregulated in human breast and ovarian cancer cells and released from apoptotic tumor c

106 Notably, reintroduction of CIB2 in ovarian cancer cells blocked plasma membrane localizatio

107 l that EMT can be induced in epithelial-like ovarian cancer cells by co-expressing constitutively act

108 find that ARID1B knockdown in ARID1A mutant ovarian cancer cells causes similar loss of enhancer arc

109 bition of cell proliferation was observed in ovarian cancer cells compared to CHOK1.

110 Silencing GPAM in ovarian cancer cells decreased cell migration and reduce

111 we showed that acquired cisplatin-resistant ovarian cancer cells expressed high levels of MKP-1 and

112 the tumor growth and migratory phenotypes of ovarian cancer cells expressing SHMT1 shRNAs.

113 aneously implanted cisplatin-resistant human ovarian cancer cells in athymic nude mice.

114 pithelial-to-mesenchymal transition (EMT) of ovarian cancer cells in vivo, STAT4 failed to induce EMT

115 wever, molecular mechanism sustaining EMT of ovarian cancer cells remains elusive.

116 parib) while overexpression of USP13 renders ovarian cancer cells resistant to chemotherapy.

117 ntiproliferative behavior against epithelial ovarian cancer cells resistant to cisplatin.

118 Thus, ovarian cancer cells seem to display heterogeneity in us

119 gulation of metastasis-associated behaviors, ovarian cancer cells that express low endogenous levels

120 s and reverses multi-drug resistance against ovarian cancer cells through downregulation of survivin.

121 apeutics, expression of CIB2 also sensitized ovarian cancer cells to carboplatin.

122 Depleting or inhibiting USP13 sensitizes ovarian cancer cells to cisplatin and PARP inhibitor (ol

123 To evaluate whether the response of ovarian cancer cells to pitavastatin is potentiated by f

124 how inhibiting DNA methylation can sensitize ovarian cancer cells to platinum drugs, in large part by

125 itaxel (PTX) and doxorubicin (DOX) resistant ovarian cancer cells to PTX and DOX by inhibiting surviv

126 Co-incubation of ovarian cancer cells with ascites fluid significantly in

127 Using pancreatic and ovarian cancer cells with ST6Gal-I knockdown or overexpr

128 In the patient derived ovarian cancer cells, a similar correlation was observed

129 st of mesenchymal traits in mesenchymal-like ovarian cancer cells, whereas expressing constitutively

130 its clonal growth, migration and invasion of ovarian cancer cells, whereas silencing in vivo inhibits

131 is and suppressing migration and invasion in ovarian cancer cells, which indicates its therapeutic po

132 cid, risedronate and GGTI-2133 in a panel of ovarian cancer cells.

133 r with ERalpha/ERbeta-expressing SKOV3 human ovarian cancer cells.

134 active Rac1 leads to EMT in epithelial-like ovarian cancer cells.

135 lass I and class II molecules exclusively on ovarian cancer cells.

136 plex is critical for sustained EMT traits of ovarian cancer cells.

137 d in vitro against both multiple myeloma and ovarian cancer cells.

138 ociated neovasculature and on the surface of ovarian cancer cells.

139 n resulted in reduced SHMT1 transcription in ovarian cancer cells.

140 C transcriptomic profiles (Classification of Ovarian Cancer [CLOVAR]), and to develop an imaging-base

141 ysis of 7 nested case-control studies in the Ovarian Cancer Cohort Consortium to investigate the asso

142 0 scores, were associated with lower risk of ovarian cancer (comparing the highest quartile (4th) vs.

143 cancer screening studies, low prevalence of ovarian cancer consistently resulted in low positive pre

144 try-Medicare data, we assessed patients with ovarian cancer deceased in 2000 to 2012 with at least 13

145 eted imaging with the potential to transform ovarian cancer detection.

146 I-MS as a powerful approach for rapid serous ovarian cancer diagnosis based on altered metabolic sign

147 (NSAIDs) rank just as high as currently used ovarian cancer drugs.

148 acterization further supports the DNM3OS and ovarian cancer EMT connection.

149 on and their reproducible gene regulation in ovarian cancer EMT.

150 Despite clinical remission of epithelial ovarian cancer (EOC) after surgical resection and first-

151 studies of Myc family targets in epithelial ovarian cancer (EOC) and neuroblastoma.

152 Epithelial ovarian cancer (EOC) has poor prognosis and rapid recurr

153 drug-repositioning candidates for epithelial ovarian cancer (EOC) have not been undertaken.

154 Epithelial ovarian cancer (EOC) is characterized by an immune suppr

155 Epithelial ovarian cancer (EOC) is one of the most common gynecolog

156 Epithelial ovarian cancer (EOC) is the most fatal gynaecological ma

157 Epithelial ovarian cancer (EOC) is the most lethal gynaecological m

158 Invasive epithelial ovarian cancer (EOC) is the most lethal gynecologic mali

159 During epithelial ovarian cancer (EOC) progression, intraperitoneally diss

160 ociation between hysterectomy and epithelial ovarian cancer (EOC) was considered well established, in

161 e with prognosis in patients with epithelial ovarian cancer (EOC), but their prognostic importance an

162 therapy (NACT) for advanced-stage epithelial ovarian cancer (EOC).

163 n several solid tumors, including epithelial ovarian cancer (EOC).

164 ngiogenesis) inhibitors such as pazopanib in ovarian cancer even when (18)F-FDG PET/CT does not indic

165 We demonstrate that ovarian cancer exhibits a targetable alteration in iron

166 ue microarray analysis revealed that >98% of ovarian cancers express the prolactin receptor (PRLR), f

167 rd of care for women with platinum-sensitive ovarian cancer following a complete or partial response

168 evel, we integrated protein and mRNA data of ovarian cancer from The Cancer Genome Atlas (TCGA) and C

169 Furthermore, UBR5 expression was higher in ovarian cancers from cisplatin-resistant patients than f

170 Ovarian cancer G protein coupled receptor 1 (OGR1, aka G

171 Analysis of ovarian cancer gene microarray data showed that higher e

172 In addition, KDM3A induces ovarian cancer growth while antagonizing cellular senesc

173 ,361 females enrolled in prostate cancer and ovarian cancer GWAS.

174 wever, the mechanism of Nectin-4 cleavage in ovarian cancer has not yet been determined.

175 Mortality rates for ovarian cancer have declined only slightly in the past f

176 inhibit certain tumor cell lines, including ovarian cancer, hepatocarcinoma and retinoblastoma, thro

177 ovarian and other cancers.High-grade serous ovarian cancers (HGS-OvCa) frequently develop chemothera

178 fective chemotherapies for high-grade serous ovarian cancers (HGS-OvCa) has motivated a search for al

179 mutations in patients with high-grade serous ovarian cancer (HGSC) are associated with favorable resp

180 High-grade serous ovarian cancer (HGSC) is an aggressive cancer with a wor

181 progenitor populations for high-grade serous ovarian cancer (HGSC).

182 ed in approximately 30% of high-grade serous ovarian cancer (HGSOC) patients and is a recurrent lesio

183 y (CT) imaging features of high-grade serous ovarian cancer (HGSOC), to assess their associations wit

184 biomarkers for olaparib in high-grade serous ovarian cancer (HGSOC).

185 specially in patients with high-grade serous ovarian cancer (HGSOC).

186 In human ovarian cancers, high PRKCI expression also correlates w

187 nd potent antitumor efficacy in an ES-2-luc, ovarian cancer i.p. xenograft model.

188 metrial cancer in 53 of 196 (27%) women; and ovarian cancer in 15 (8%) of 196 women.

189 endometrial cancer in 83 (30%) of 279 women; ovarian cancer in 28 (10%) of 279 women; and colorectal

190 formed at the Center for Familial Breast and Ovarian Cancer in Cologne, Germany; data analysis, Novem

191 outcomes in platinum-resistant and recurrent ovarian cancer in part by effects on DNA repair and anti

192 by identifying patients with advanced-stage ovarian cancer in whom > 1 cm of residual disease will b

193 Ovarian cancer is a highly aggressive disease and novel

194 Epithelial ovarian cancer is a leading cause of death in gynecologi

195 Ovarian cancer is a lethal malignancy that has not seen

196 fibroblasts (CAFs) confer chemoresistance in ovarian cancer is poorly understood.

197 The current standard care of ovarian cancer is still cytoredutive surgery followed by

198 Ovarian cancer is the leading cause of death among all g

199 High-grade serous ovarian cancer is the most common ovarian cancer type.

200 Ovarian cancer is the most leading cause of cancer-relat

201 Ovarian cancer is usually diagnosed after metastasis.

202 d that ID8, a widely-used syngeneic model of ovarian cancer, lacked any of the frequent mutations in

203 d BRCA2 mutations are frequent in women with ovarian cancer, many such women have not been tested, es

204 4 patients with pathologically proven serous ovarian cancer (mean age +/- standard deviation, 59 year

205 n with endometrial cancer, and 49 women with ovarian cancer; mean follow-up was 68.2 months.

206 ential key transcription factors involved in ovarian cancer metastasis and identified STAT4 as a crit

207 tudy established a model that STAT4 promotes ovarian cancer metastasis via tumor-derived Wnt7a-induce

208 and identified STAT4 as a critical player in ovarian cancer metastasis.

209 function as a regulatory mechanism to impact ovarian cancer metastatic success.

210 nstrate the visualization of intraperitoneal ovarian cancer micrometastasis as small as 100 mum with

211 ancers which can aid in the visualization of ovarian cancer micrometastasis.

212 Our results demonstrate in colon and ovarian cancer models that an oncolytic vaccinia virus a

213 Lastly, in ovarian cancer models, key proteins that coordinate reco

214 ere we report an integrated analysis of >700 ovarian cancer molecular profiles, including genomic dat

215 end = 0.002) and a positive association with ovarian cancer mortality (HR, 1.31 [CI, 1.07 to 1.61]; P

216 ra-red fluorescence (NIRF) imaging on SKOV-3 ovarian cancer mouse model demonstrated that the NIR dye

217 Here, we show that in advanced ovarian cancers NFkappaB signaling via the RelB transcri

218 pecifically to N-glycans present on 11 of 19 ovarian cancer (OC) and 8 of 14 breast cancer cell lines

219 Ovarian cancer (OC) is the most deadly gynecological can

220 l sonography (TVS) for women at high risk of ovarian cancer (OC) or fallopian tube cancer (FTC).

221 ant risk genes for breast cancer (BC) and/or ovarian cancer (OC), including BRCA1 and BRCA2, explain

222 llion women have a history of breast (BC) or ovarian cancer (OC).

223 the mutation landscape of serous epithelial ovarian cancer, other non-serous subtypes of the disease

224 In high-grade serous ovarian cancer (OV), the bulk of genetic changes is not

225 e investigated its role in Akt activation in ovarian cancer (OVCa) cell lines (OVCAR-3, SKOV-3, and C

226 Ovarian cancer (OvCa) cells are reported to undergo bioc

227 er Genome Atlas mRNA expression data for HGS ovarian cancer patient samples, we observed that six enz

228 use of targeted PARP-inhibitor therapies in ovarian cancer patients carrying deleterious missense RA

229 In ovarian cancer patients treated with bevacizumab, serum

230 ce treatment in platinum-sensitive, relapsed ovarian cancer patients with a BRCA1/2 mutation who had

231 sh UBC as a promising therapeutic target for ovarian cancer patients with recurrent UBB silencing.

232 In matched samples from 11 high-grade serous ovarian cancer patients, we detected 2-20-fold more sN4

233 stress on chemosensitivity and prognosis of ovarian cancer patients.

234 ases, and ascites cells isolated from serous ovarian cancer patients.

235 ose abundance was increased in the plasma of ovarian cancer patients.

236 e personalized care and survival outcomes of ovarian cancer patients.Significance: Epigenomic targeti

237 ons may present with a hereditary breast and ovarian cancer phenotype.

238 tanding the function of Nectin-4 shedding in ovarian cancer progression is critical to facilitate its

239 r pathways/transcription factors involved in ovarian cancer progression, poor clinical outcome, and c

240 ts an effective therapeutic strategy against ovarian cancer progression.

241 proposed to be a pivotal cytokine promoting ovarian cancer progression.

242 an abnormal screening pelvic examination for ovarian cancer ranged from 5% to 36% at 1 year, with the

243 nknown adnexal cysts at CT was 6.6%, with an ovarian cancer rate of 0.7% (95% CI: 0.4%, 1.0%).

244 ublets are a standard of care for women with ovarian cancer recurring 6 months after completion of in

245 (HGS) ovarian cancer accounts for 90% of all ovarian cancer-related deaths.

246 Ovarian cancer remains the most lethal gynecological mal

247 that is broadly over-expressed in breast and ovarian cancer, remains unknown.

248 etween pelvic inflammatory disease (PID) and ovarian cancer risk are few and inconsistent.

249 n overall healthy dietary pattern may reduce ovarian cancer risk in African-American women, and parti

250 lthy Eating Index (AHEI)-2010-in relation to ovarian cancer risk in African-American women.

251 iation with PID, the association of PID with ovarian cancer risk is still somewhat uncertain and requ

252 No association was observed between PID and ovarian cancer risk overall (pOR = 0.99, 95% CI: 0.83, 1

253 The cumulative ovarian cancer risk to age 80 years was 44% (95% CI, 36%

254 een quartiles of dietary quality indices and ovarian cancer risk, adjusting for potential confounders

255 metabolic pathway were overexpressed in HGS ovarian cancer samples compared with normal ovary sample

256 In the 4 ovarian cancer screening studies, low prevalence of ovar

257 s) and 80,672 Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (PLCO) ever-smoking parti

258 ut the PLCO (Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial) found no reduction.

259 ansgenic mouse studies establish PRKCI as an ovarian cancer-specific oncogene.

260 formation of PGCCs and dedifferentiation in ovarian cancer specimens from patients treated with chem

261 ly increased levels of unsaturated lipids in ovarian cancer stem cells (CSCs) as compared to non-CSCs

262 platinum- resistant ovarian cancer cells and ovarian cancer stem cells and (ii) downregulation of bet

263 latinum therapy and was effective in killing ovarian cancer stem cells that contribute to both platin

264 demethylase KDM3A as a critical regulator of ovarian cancer stemness and cisplatin resistance by indu

265 logical meaningful processes associated with ovarian cancer, such as CCL11, CCL16, CCL18, CCL23, CCL8

266 Only 40% of patients with advanced ovarian cancer survive more than 5 years.

267 We have identified novel lncRNAs in ovarian cancer that are differentially expressed in CAFs

268 Poor prognosis of ovarian cancer, the deadliest of the gynecologic maligna

269 sive boronate crosslinked micelles (BCM) for ovarian cancer therapy.

270 ition to providing a potential biomarker for ovarian cancer, this approach is generally applicable to

271 racellular iron reduces the proliferation of ovarian cancer TICs in vitro, and inhibits both tumor gr

272 We show that the iron dependence of ovarian cancer TICs renders them exquisitely sensitive i

273 copy, can serve as indicators of response in ovarian cancer to multityrosine kinase inhibitor pazopan

274 uppressive microenvironment, and response of ovarian cancers to immune therapies has thus far been di

275 nal case of a patient with high-grade serous ovarian cancer, treated with multiple chemotherapy regim

276 NP(BTZ-DOX) exhibited significantly improved ovarian cancer treatment in SKOV-3 xenograft mouse model

277 may be an attractive therapeutic target for ovarian cancer treatment.

278 cision therapy opportunity for effective HGS ovarian cancer treatment.

279 otential clinical implications in breast and ovarian cancer treatment.

280 thyl transferase 1 (SHMT1) was necessary for ovarian cancer tumor growth and cell migration in cultur

281 ve analysis of the metabolic requirements of ovarian cancer tumor growth has not been performed.

282 However, factors that drive HGS ovarian cancer tumor growth have not been fully elucidat

283 eased TFR1 is observed in a genetic model of ovarian cancer tumor-initiating cells (TICs).

284 -omics profiles of primary high-grade serous ovarian cancer tumours (N=357) to delineate mechanisms u

285 s explored against orthotopic pancreatic and ovarian cancer tumours.

286 ade serous ovarian cancer is the most common ovarian cancer type.

287 onment could enable peritoneal metastasis of ovarian cancer via induction of EMT program.

288 results showed that mRNA levels of IL-6R in ovarian cancer was positively associated with better pro

289 ment of drug resistance in high-grade serous ovarian cancer, were examined from patient derived malig

290 subset of common types of cancer, including ovarian cancer, where NAPRT expression correlates with a

291 l opportunity to identify driver patterns in ovarian cancer, which will acquire some novel and clinic

292 survival in patients with platinum-sensitive ovarian cancer who had achieved a response to platinum-b

293 Patients with suspected advanced-stage ovarian cancer who qualified for PCS were eligible.

294 ients with BRCA wild-type platinum-sensitive ovarian cancers who might benefit from rucaparib.

295 e-associated colorectal, endometrial, and/or ovarian cancers whose medical records were included in t

296 nalysis on the results for high-grade serous ovarian cancer with the results from analysis of 31,448

297 Rucaparib is approved for recurrent ovarian cancers with germline or somatic mutations in BR

298 In a luciferase-expressing ES-2 (ES-2-luc) ovarian cancer xenograft model, single i.p. injections o

299 analyzed 12 treatment groups in trial on an ovarian cancer xenograft, reproducing current therapeuti

300 hown that pitavastatin induces regression of ovarian cancer xenografts in mice.