ライフサイエンスコーパス: ovarian cancer cell line

1 ombination in vitro and in vivo with a human ovarian cancer cell line.

2 el supported by in vitro experiments with an ovarian cancer cell line.

3 t was highly expressed in Hey, an epithelial ovarian cancer cell line.

4 epigenetic treatments on a human epithelial ovarian cancer cell line.

5 he effects of semaphorin 3B on HEY cells, an ovarian cancer cell line.

6 inoculated with the DF3-positive 36M2 human ovarian cancer cell line.

7 l extent of a homozygous deletion in another ovarian cancer cell line.

8 isplay to amplify related mRNAs from a human ovarian cancer cell line.

9 H1 variants, H1.3, in the OVCAR-3 epithelial ovarian cancer cell line.

10 luated in 119 primary ovarian cancers and 12 ovarian cancer cell lines.

11 uccessfully targeted to increase response in ovarian cancer cell lines.

12 cancers were subject to targeted therapy in ovarian cancer cell lines.

13 etween PKCiota and cyclin E in a panel of 19 ovarian cancer cell lines.

14 ChNKG2D-expressing T cells lysed ovarian cancer cell lines.

15 activity against HL-60 leukemia and OVCAR-3 ovarian cancer cell lines.

16 nd GATA4 expression is absent in majority of ovarian cancer cell lines.

17 e of origin and histopathology of epithelial ovarian cancer cell lines.

18 s a potent inducer of GROalpha expression in ovarian cancer cell lines.

19 om two distinct genetically engineered mouse ovarian cancer cell lines.

20 ular matrix constituents by murine and human ovarian cancer cell lines.

21 induced cytotoxicity in paclitaxel-resistant ovarian cancer cell lines.

22 n epithelial cells as well as in four of six ovarian cancer cell lines.

23 rrelated with higher levels of ERCC1 mRNA in ovarian cancer cell lines.

24 eath in both wild-type p53 and p53-deficient ovarian cancer cell lines.

25 xic (nM IC(50)s) against cisplatin-resistant ovarian cancer cell lines.

26 n of HtrA1 is downregulated in five of seven ovarian cancer cell lines.

27 ge of caspase substrates, in six low-passage ovarian cancer cell lines.

28 d7 transcription in breast, endometrial, and ovarian cancer cell lines.

29 stage ovarian cancer specimens and in all 17 ovarian cancer cell lines.

30 of its frequent loss of expression (LOE) in ovarian cancer cell lines.

31 ctors that were strongly activated by LPA in ovarian cancer cell lines.

32 not detected in the majority of established ovarian cancer cell lines.

33 rian epithelial cells (IOSE) and compared to ovarian cancer cell lines.

34 either overexpressed or silenced in several ovarian cancer cell lines.

35 for antitumor activity in both leukemia and ovarian cancer cell lines.

36 pression of MCJ was absent in three of seven ovarian cancer cell lines.

37 inum(II) complexes for both PA-1 and SK-OV-3 ovarian cancer cell lines.

38 d a low Fas/FAP-1 ratio (P: < or = 0.028) in ovarian cancer cell lines.

39 as induced by Wee1 inhibition in breast and ovarian cancer cell lines.

40 I ratio in 7 HOSE cultures relative to eight ovarian cancer cell lines.

41 nduced upregulation of Muc-1 on prostate and ovarian cancer cell lines.

42 d its expression and mutational status in 13 ovarian cancer cell lines.

43 opic GPC3 expression inhibited the growth of ovarian cancer cell lines.

44 cinoma primary cell cultures and established ovarian cancer cell lines.

45 e show that IL-4R is expressed by breast and ovarian cancer cell lines.

46 f five estrogen receptor-positive breast and ovarian cancer cell lines.

47 ormal ovary and tumor samples and epithelial ovarian cancer cell lines.

48 mples and with cisplatin resistance in human ovarian cancer cell lines.

49 models of ovarian cancer and in other human ovarian cancer cell lines.

50 As) that are active against a panel of human ovarian cancer cell lines.

51 ignant human ovarian tumors as well as human ovarian cancer cell lines.

52 ry tumors or differentially overexpressed in ovarian cancer cell lines.

53 y synergized with FdUrd but not with 5-FU in ovarian cancer cell lines.

54 re associated with neoplastic suppression in ovarian cancer cell lines.

55 MH between cisplatin sensitive and resistant ovarian cancer cell lines.

56 Of the 39 ovarian cancer cell lines, 14 were assigned as high-grad

57 B to inhibit HIF-1alpha protein in the human ovarian cancer cell line 1A9 and its beta-tubulin mutant

58 Two paclitaxel(Ptx)-resistant ovarian cancer cell lines, 1A9/Ptx-10 and 1A9/Ptx-22, is

59 -regulation of p21(WAF1/CIP1) within a human ovarian cancer cell line, 2774, and the derivative cell

60 10 x 10(6) cells from a CD44-positive human ovarian cancer cell line (36M2) in the presence of eithe

61 ion of the CpG island and SNCG expression in ovarian cancer cell lines (5 of 5).

62 cell death in the cisplatin-sensitive human ovarian cancer cell line A2780 and two drug-resistant su

63 The mutation frequency of the ovarian cancer cell line A2780, analyzed at the HPRT loc

64 ection for cisplatin resistance in the human ovarian cancer cell line A2780, results in loss of expre

65 ts and HDAC inhibitory activity in the human ovarian cancer cell line A2780, the human squamous carci

66 on of colony formation was quantified in the ovarian cancer cell line A2780, where it was demonstrate

67 We studied the paired human ovarian cancer cell lines A2780 and A2780-CP70.

68 ePt NPs can bind preferentially to the human ovarian cancer cell line (A2780) that overexpresses LHRH

69 splatin caused an activation of autophagy in ovarian cancer cell lines, A2780, OVCAR3 and SKOV3.

70 minescence signals from ES-2 and SKOV3 human ovarian cancer cell lines after IP injection.

71 In the ovarian cancer cell lines, AG490 also diminished the pho

72 AD1 and AD2 is absent in certain breast and ovarian cancer cell lines, although each domain can stil

73 We have isolated from multiple ovarian cancer cell lines an ovarian cancer stem cell-en

74 In five ovarian cancer cell lines analysed, four did not express

75 growth inhibition in both a human epithelial ovarian cancer cell line and a cell line derived from no

76 NVs) as small as 30 kb in single cells of an ovarian cancer cell line and as small as 9 Mb in two hig

77 A paclitaxel-resistant human ovarian cancer cell line and its parental line both resp

78 usly to have a direct antitumor effect on an ovarian cancer cell line and ovarian carcinoma cells iso

79 To explore the expression of FAP-1 in ovarian cancer cell lines and archival tumor specimens,

80 A (siRNA) to silence its expression in human ovarian cancer cell lines and assessed the effects of it

81 netic changes typical of those seen in HGSOC ovarian cancer cell lines and biopsies.

82 DH1-bright (ALDH1(br)) cells from epithelial ovarian cancer cell lines and characterized the properti

83 APOBEC3B is active in the nucleus of several ovarian cancer cell lines and elicits a biochemical pref

84 CYP1A1v is overexpressed in ovarian cancer cell lines and exhibits a unique subcellu

85 s of established human prostate, breast, and ovarian cancer cell lines and found that all cancer cell

86 rapamil-sensitive SPs in three of four human ovarian cancer cell lines and four of six patient primar

87 in molecular profiles between commonly used ovarian cancer cell lines and high-grade serous ovarian

88 Here we analyse a panel of 47 ovarian cancer cell lines and identify those that have t

89 sing isogenic, cisplatin-sensitive/resistant ovarian cancer cell lines and inducing resensitizaton wi

90 relates significantly with Fas resistance in ovarian cancer cell lines and is commonly expressed in o

91 d by transfecting the full-length gene in to ovarian cancer cell lines and no suppression of growth w

92 full-length MUC1/TM expressed by breast and ovarian cancer cell lines and on freshly obtained, unman

93 and sufficient for paclitaxel resistance in ovarian cancer cell lines and ovarian tumor explants.

94 Stimulation of ovarian cancer cell lines and primary epithelial cancer

95 purification and culture of PGCCs from human ovarian cancer cell lines and primary ovarian cancer.

96 on with antibodies revealed that most of the ovarian cancer cell lines and primary tumors had diminis

97 (Pol eta) in ovarian CSCs isolated from both ovarian cancer cell lines and primary tumors, indicating

98 stone acetylation of HSulf-1 was analysed in ovarian cancer cell lines and primary tumors.

99 nal/exon rearrangement analysis of Parkin in ovarian cancer cell lines and primary tumors.

100 quently overexpressed and activated in human ovarian cancer cell lines and primary tumors.

101 anel of multiple myeloma, neuroblastoma, and ovarian cancer cell lines and showed that SylA-GlbA stro

102 sslinking agents, and has been identified in ovarian cancer cell lines and sporadic primary tumor tis

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

104 and quantitative (phospho-)proteomes of five ovarian cancer cell lines and the global cancer genome r

105 e epithelial (HOSE) cell cultures but not in ovarian cancer cell lines and tissues.

106 p-regulate the Maspin promoter in aggressive ovarian cancer cell lines and to interrogate the therape

107 w that HOXB13 is expressed in multiple human ovarian cancer cell lines and tumors and that knockdown

108 multi-isoform genes in a stem cell line, an ovarian cancer cell line, and a breast cancer cell line

109 an active catalytic subunit of PI3k into an ovarian cancer cell line, and thus activation of the PI3

110 These loops operate in several ovarian cancer cell lines, and BRCA1-IRIS silencing or i

111 sion and acquired cisplatin resistance among ovarian cancer cell lines, and genetic knockout of CTR1

112 shared among human ovarian primary cancers, ovarian cancer cell lines, and normal fimbria.

113 f-1 was up-regulated in paclitaxel-resistant ovarian cancer cell lines, and Rsf-1 immunoreactivity in

114 was found to be overexpressed in 4 out of 6 ovarian cancer cell lines as compared with an immortaliz

115 Using human ovarian cancer cell lines as well as malignant epithelia

116 and carboplatin on 10 different cervical and ovarian cancer cell lines as well as on the ability of t

117 t GPR55 is expressed in several prostate and ovarian cancer cell lines, both at the mRNA and at the p

118 ere are approximately 100 publicly available ovarian cancer cell lines but their cellular and molecul

119 TF was expressed in four of the five ovarian cancer cell lines, but absent in the nontransfor

120 overexpressed in several cisplatin-resistant ovarian cancer cell lines, but its relationship to resis

121 arian carcinomas, and in the CAOV3 and SKOV3 ovarian cancer cell lines, but not in normal ovarian sur

122 roliferative activity toward the A2780 human ovarian cancer cell line by the cis and trans analogues

123 It is expressed in 4/8 ovarian cancer cell lines by Northern analysis.

124 l, ineffective against Taxol-resistant human ovarian cancer cell lines, can be incorporated into a re

125 Ovarian cancer cell lines Caov-3, OVCAR-3, SK-OV-3, UCI-

126 Specifically, we showed that in the human ovarian cancer cell lines, cisplatin induces MKP-1 throu

127 mately 50-fold more toxic in the A2780 human ovarian cancer cell line compared with clones of the HCT

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

129 o 80%) on transfecting these siRNAs into the ovarian cancer cell line CP70.

130 wed that IKK-epsilon depletion in metastatic ovarian cancer cell lines decreased growth, adhesion, an

131 ts done by expressing kinase-dead CHK2 in an ovarian cancer cell line demonstrated that CHK2 activati

132 time-dependent manner in multiple breast and ovarian cancer cell lines demonstrated by a T421/S424 ph

133 Conversely, silencing BRCA1-IRIS in ovarian cancer cell lines derepressed PTEN expression al

134 have examined a panel of 12 unrelated human ovarian cancer cell lines derived from patients who were

135 We generated several novel murine ovarian cancer cell lines derived from the ovarian surfa

136 However, siRNA inactivation of claudins in ovarian cancer cell lines did not have a significant eff

137 rect sequencing of the gene in all the eight ovarian cancer cell lines did not identify any mutations

138 y more cytotoxic than 4 in a number of human ovarian cancer cell lines (e.g., IC(50) values of 0.0225

139 nd cell cycle distribution profiles of three ovarian cancer cell lines (ES-2, PA-1 and NIH OVCAR-3) t

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

141 gion of chromosome 22q deleted in 47% of the ovarian cancer cell lines examined.

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

143 The Ovcar-5 and Skov-3 ovarian cancer cell lines exposed to the Ad-Lp-CD adenov

144 We previously demonstrated that ovarian cancer cell lines express high levels of constit

145 istant human (CaOV3TaxR) and mouse (ID8TaxR) ovarian cancer cell lines express large amounts of the m

146 In NIH:OVCAR-5, the only ovarian cancer cell line expressing COX-2, signal pathwa

147 Finally, breast and ovarian cancer cell lines expressing an acetylation mime

148 in vitro and in vivo against human and mouse ovarian cancer cell lines expressing MIS type II recepto

149 ions cisplatin failed to induce apoptosis in ovarian cancer cell lines expressing this regulatory cas

150 bition of MYCC or MYC paralogs in a panel of ovarian cancer cell lines expressing varying levels of M

151 in the peritoneal cavity, whereas aggressive ovarian cancer cell lines failed to form tumors or metas

152 hway may promote oncogenesis, we examined 10 ovarian cancer cell lines for resistance to cytochrome c

153 anel of normal and tumor ovarian tissues and ovarian cancer cell lines for the expression of Rb, p16

154 LSCR1 cDNA was stably expressed in the human ovarian cancer cell line HEY1B, and the growth of these

155 d depletion of endogenous RNase L in a human ovarian cancer cell line (Hey1b) increased the levels of

156 pic implantation of the human drug-resistant ovarian cancer cell line HeyA8-MDR, followed by porous s

157 port the integrated proteomic analysis of 26 ovarian cancer cell lines, HGSOC tumours, immortalized o

158 an invasive variant of the murine epithelial ovarian cancer cell line ID8-T.

159 vaccine using whole cell lysate of a murine ovarian cancer cell line, ID8 was prepared by spray dryi

160 aring normal ovarian epithelial cultures and ovarian cancer cell lines identified pregnancy-associate

161 odel of ABT-737 and carboplatin action on an ovarian cancer cell line (IGROV-1).

162 used intraperitoneal xenografts of the human ovarian cancer cell line IGROV1-Luc in Balb/c nude mice,

163 tive, nanomolar activity against OVCAR-3, an ovarian cancer cell line in the National Cancer Institut

164 atin's ability to induce tumor cell death in ovarian cancer cell line in vitro and in vivo.

165 ect the proliferation of a receptor-negative ovarian cancer cell line in vitro.

166 Ovarian cancer cell lines in culture express and secrete

167 We measured IL-6 production by human ovarian cancer cell lines in vitro and in vivo.

168 es the ovary, and MIS inhibits the growth of ovarian cancer cell lines in vitro, suggesting a key rol

169 We detected CD133 on ovarian cancer cell lines, in primary cancers and on pur

170 lf suppressed colony formation in breast and ovarian cancer cell lines, in which E1A is known to have

171 tors PP242 or rapamycin-sensitized DOV13, an ovarian cancer cell line incapable of inducing REDD1, to

172 nt or very low in the majority of breast and ovarian cancer cell lines, including MCF-7 and SK-Br-3 b

173 expression of IKK-epsilon in a less invasive ovarian cancer cell line increased metastasis in vivo.

174 n embryonal carcinoma cell lines with breast/ovarian cancer cell lines indicates that DNMT3A2 express

175 he effects of HMGB1 overexpression in a BG-1 ovarian cancer cell line, induced by steroid hormones, o

176 that re-expression of ARHI in multiple human ovarian cancer cell lines induces autophagy by blocking

177 dogenous HOXB13 by RNA interference in human ovarian cancer cell lines is associated with reduced cel

178 er cell line SNB-75 (GI(5)(0) = 0.0159 muM), ovarian cancer cell line NCI/ADR-RES (GI(5)(0) = 0.0169

179 rom a breast cancer cell line, MCF-7, and an ovarian cancer cell line, NCI/ADR-RES, and by using geno

180 d colorectal cancer cells and the unexplored ovarian cancer cell line NIH:OVCAR-3, with respective PN

181 binding and uptake were studied with a human ovarian cancer cell line, NIH-OVCAR-5, and a nonantigen-

182 valuated for anticancer activity against the ovarian cancer cell line NuTu-19 and for cell toxicity a

183 underlying molecular mechanisms in a murine ovarian cancer cell line, OCA-I.

184 decrease in cell proliferation rate in three ovarian cancer cell lines on treatment with retinoic aci

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

186 was not expressed in four of 11 (36%) human ovarian cancer cell lines or spontaneously transformed h

187 As such, an ovarian cancer cell line, OV-90, was cultured in adheren

188 , we introduced EGFRvIII into the epithelial ovarian cancer cell line OVCA 433.

189 te, resulted in a decrease in TJ strength in ovarian cancer cell line OVCA433.

190 he tumorigenicity of the low-HER2-expressing ovarian cancer cell line OVCAR-3 by decreasing cell prol

191 ubsequent light-triggered death in the human ovarian cancer cell line OVCAR-5.

192 onor 3-morpholino-sydnonimine toward a human ovarian cancer cell line (OVCAR) was examined.

193 motifs were identified and validated from an ovarian cancer cell line (OVCAR-3).

194 he relative phototoxicity in vitro toward an ovarian cancer cell line (OVCAR-5) while reducing it tow

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

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

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

198 e arrest and apoptosis in an apoE-expressing ovarian cancer cell line, OVCAR3, but not in apoE-negati

199 me 11 (chr 11) to a clonal derivative of the ovarian cancer cell line, OVCAR3, was performed and gene

200 In contrast, ovarian cancer cell lines OVCAR4 and OVCAR5, which have

201 As in the ovarian cancer cell line OVCAR8, suppression of growth o

202 ration/survival of both an established human ovarian cancer cell line (OVCAR8) and a subset of primar

203 -downregulated clones, IOSE-523 and in other ovarian cancer cell lines (OVCAR8, SKOV3ip and DOV13), s

204 All three ovarian cancer cell lines overexpressed FAK compared to

205 l cultures was 4.1 compared with 270.4 in 14 ovarian cancer cell lines (P =.03).

206 degradation by the human HPV E6 gene in the ovarian cancer cell line PA1 leads to an increase in the

207 In the human ovarian cancer cell line PA1, XK469 caused the release o

208 In contrast, the human ovarian cancer cell line, PA1, failed to express hTR4alp

209 ian surface epithelial (HOSE) cell lines, 13 ovarian cancer cell lines, paraffin blocks (n = 84), and

210 Three ovarian cancer cell lines (PEO1, PEO4, and PEO6) were de

211 own of claudin-3 and claudin-4 expression in ovarian cancer cell lines reduced invasion.

212 ated that the levels of FER were elevated in ovarian cancer cell lines relative to those in immortali

213 Re-expression of HSulf-1 in ovarian cancer cell lines resulted in diminished HSPG su

214 ncing of HSulf-1 in OV202 and TOV2223 cells (ovarian cancer cell lines) resulted in increased lipid d

215 wn-regulation of HS6ST-1 or HS6ST-2 in human ovarian cancer cell lines results in 30-50% reduction in

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

217 In vitro and in vivo studies involving ovarian cancer cell lines revealed that expression of LO

218 In general, ovarian cancer cell lines showed relatively high levels

219 ast overexpression of ectopic p16 in the one ovarian cancer cell line (SK-OV-3) that expressed Rb but

220 cer cell lines (H460, H322, H520, H661), two ovarian cancer cell lines (SK-OV-03, A2780), cervical ca

221 ol-resistant subline, derived from the human ovarian cancer cell line SKOV-3, was established through

222 as transferred into the malignant epithelial ovarian cancer cell line, SKOv-3, by microcell-mediated

223 Targeted KLF6 reduction in an ovarian cancer cell line, SKOV-3, resulted in a 50% redu

224 ed in pcDNA3.1 was expressed in a MUC13 null ovarian cancer cell line, SKOV-3.

225 otic signaling and overcome MDR in the human ovarian cancer cell line SKOV3.

226 lls (HEK293([SCL60])) with transfected human ovarian cancer cell lines SKOV3 and EFO21, human hepatob

227 tants with that of parental cells in a human ovarian cancer cell line (SKOV3.ip1); we found that the

228 ted nonkinase (FRNK) was introduced into two ovarian cancer cell lines (SKOV3 and 222).

229 was to further characterize an endometrioid ovarian cancer cell line, SNU-251, which was previously

230 HSV-TK) under OSP-1 control was sufficiently ovarian cancer cell line specific to render ganciclovir

231 ncated dominant negative BRCA1 on breast and ovarian cancer cell lines subjected to a number of diffe

232 Re-expression of RPS6KA2 in ovarian cancer cell lines suppressed colony formation.

233 nction of ERBB4 in each breast, prostate and ovarian cancer cell line tested.

234 e inhibits growth in vitro of all breast and ovarian cancer cell lines tested, but not colon or lung

235 76 abolished LPA-induced uPA upregulation in ovarian cancer cell lines tested, indicating the importa

236 In SKOV-3 cells (a human ovarian cancer cell line that contains high levels of wi

237 Using an UNG2-deficient ovarian cancer cell line that is hypersensitive to floxu

238 G protein-coupled receptor 1 (OGR1), from an ovarian cancer cell line that maps to chromosome 14q31.

239 on and anchorage-independent growth in mouse ovarian cancer cell lines that contain genetic alteratio

240 When compared with two ovarian cancer cell lines that did not make TNF-alpha, c

241 ing reverse transcription-PCR, we identified ovarian cancer cell lines that endogenously overexpress

242 y of rAd-MET was tested on the OVCAR-8 human ovarian cancer cell line, the HT1080 human fibrosarcoma

243 4, CD24, and Epcam--which selected, in three ovarian cancer cell lines, those cells which best formed

244 with elevated expression in the majority of ovarian cancer cell lines (three SDs above the mean of n

245 ogy, showed migration of i.p. injected human ovarian cancer cell line to mouse ovaries.

246 B gene silencing restored the sensitivity of ovarian cancer cell lines to cisplatin in vitro.

247 Exposure of ovarian cancer cell lines to increasing concentrations o

248 of the pro-apoptotic protein BAX sensitizes ovarian cancer cell lines to paclitaxel in vitro by enha

249 profile molecular changes in the A2780 human ovarian cancer cell line treated with 17AAG.

250 tical for kinase activation, was observed in ovarian cancer cell lines treated with irofulven.

251 Comprehensive profiling of 39 ovarian cancer cell lines under controlled, uniform cond

252 We have characterized 39 ovarian cancer cell lines under uniform conditions for g

253 Downregulation of CtBP2 expression in ovarian cancer cell lines using short-hairpin RNA strate

254 ligonucleotide (ODN) in breast, prostate and ovarian cancer cell lines, using 32P-labeled ODN.

255 The SKOV3ip.1 human ovarian cancer cell line was chosen for these studies be

256 NuTu-19, a rat ovarian cancer cell line was rendered resistant to cispl

257 rate clonal transfectants from two different ovarian cancer cell lines was found to significantly enh

258 observed between the sensitive and resistant ovarian cancer cell lines was the result of dissimilar u

259 In this study using human ovarian cancer cell lines, we found that RB protein and

260 After reintroducing KLF2 into ovarian cancer cell lines, we observed decreased cell gr

261 ng ALDH in combination with CD133 to analyze ovarian cancer cell lines, we observed even greater grow

262 ALDH(+) cells isolated from ovarian cancer cell lines were chemoresistant and prefer

263 The data indicated that four ovarian cancer cell lines were positive for one or both

264 the influence of IL-8 on tumor growth, human ovarian cancer cell lines were transfected with an expre

265 CYP1A1 mRNA, but not CYP1B1 transcripts, in ovarian cancer cell lines when compared with primary cul

266 action [30 (70%) of 43] of breast, lung, and ovarian cancer cell lines, whereas strong expression of

267 In this study, we used the human SW626 ovarian cancer cell line, which lacks functional p53, to

268 ed apoptosis, we transfected the SW626 human ovarian cancer cell line, which lacks functional p53, wi

269 A human ovarian cancer cell line, which migrates to mouse ovarie

270 SKOV3, an ovarian cancer cell line with dysfunctional apoptosome a

271 y understood, partially owing to the lack of ovarian cancer cell lines with defective BRCA1.

272 in the MDA-MB-231 breast cancer and SK-OV-3 ovarian cancer cell lines with IC50 values of 11.0 and 2

273 ellent activity against paclitaxel-resistant ovarian cancer cell lines with mutations in beta-tubulin

274 and ZEB1 attenuated mesothelial clearance in ovarian cancer cell lines with strong activity.

275 Treatment of ovarian cancer cell lines with the methyltransferase inh

276 with a K(i) of 1.3 muM and activity against ovarian cancer cell lines with the same potency as cispl

277 Ectopic expression of testisin in a human ovarian cancer cell line without endogenous testisin exp

278 profile on pancreas, prostate, leukemia, and ovarian cancer cell line xenografts together with apopto