ライフサイエンスコーパス: ovarian carcinoma

1 or models (CT26 colon carcinoma and ID8-VEGF ovarian carcinoma).

2 ominant site of origin for high-grade serous ovarian carcinoma.

3 broader clinical utility in ERalpha-positive ovarian carcinoma.

4 patients with platinum-resistant/refractory ovarian carcinoma.

5 abeled antibody administered in vivo against ovarian carcinoma.

6 tional relevance of SOX2 expression in human ovarian carcinoma.

7 presented among miRNA genes overexpressed in ovarian carcinoma.

8 responsible for altered miRNA expression in ovarian carcinoma.

9 were not previously implicated in inherited ovarian carcinoma.

10 a group of ~30 cancer cells from a recurrent ovarian carcinoma.

11 human and murine models of BRCA1-associated ovarian carcinoma.

12 in acquired drug resistance of BRCA2-mutated ovarian carcinoma.

13 in acquired drug resistance of BRCA2-mutated ovarian carcinoma.

14 -associated macrophages in 103 patients with ovarian carcinoma.

15 hensive review of the surgical management of ovarian carcinoma.

16 e in the optimal management of all stages of ovarian carcinoma.

17 offers an attractive therapeutic approach in ovarian carcinoma.

18 all placebo-treated mice developed advanced ovarian carcinoma.

19 ethod to inhibit peritoneal dissemination of ovarian carcinoma.

20 an early event in the development of serous ovarian carcinoma.

21 th high-grade, recurrent, platinum-sensitive ovarian carcinoma.

22 relapsed peritoneal metastasis in epithelial ovarian carcinoma.

23 olonized by advanced and relapsed metastatic ovarian carcinoma.

24 NK cells and are increased in patients with ovarian carcinoma.

25 and in-house cohorts of patients with serous ovarian carcinoma.

26 h CDK12 inactivation in patients with serous ovarian carcinoma.

27 regression in the treatment of mice bearing ovarian carcinoma.

28 predicts poor prognosis in high-grade serous ovarian carcinoma.

29 s the potential as an adjuvant treatment for ovarian carcinoma.

30 ates in female nude mice bearing A2780 human ovarian carcinoma.

31 ressed in many cancers, including breast and ovarian carcinomas.

32 are the site of origin of high-grade serous ovarian carcinomas.

33 8 tumors were characteristic of human serous ovarian carcinomas.

34 e carcinomas compared with high-grade serous ovarian carcinomas.

35 XO3a in a vast majority of high-grade serous ovarian carcinomas.

36 ns may restore BRCA1/2 protein in hereditary ovarian carcinomas.

37 the leading causes of therapeutic failure in ovarian carcinomas.

38 onse to platinum chemotherapy in a subset of ovarian carcinomas.

39 nce is a serious problem in the treatment of ovarian carcinomas.

40 ons frequently occur in other major types of ovarian carcinomas.

41 duced the rejection of otherwise lethal i.p. ovarian carcinomas.

42 ibuting to tumor cell survival and growth in ovarian carcinomas.

43 l, and that its expression is deregulated in ovarian carcinomas.

44 n transgenic mice that spontaneously develop ovarian carcinomas.

45 urprisingly ineffective against SKOV-3 human ovarian carcinomas.

46 can be a potential therapeutic approach for ovarian carcinomas.

47 vant concentrations for effectively treating ovarian carcinomas.

48 versely correlated with PKM2 levels in human ovarian carcinomas.

49 AMs was a factor of poorer survival in human ovarian carcinomas.

50 hibits aberrant patterns in subsets of human ovarian carcinomas.

51 R1 and CTR2 mRNA and protein levels in human ovarian carcinoma 2008 cells and ATOX1(+/+) and ATOX1(-/

52 e CLDN3- and CLDN4-expressing parental human ovarian carcinoma 2008 cells and CLDN3 and CLDN4 knockdo

53 Knockdown of CLDN3 or CLDN4 rendered human ovarian carcinoma 2008 cells resistant to cDDP in both i

54 We found that, in the majority of ovarian carcinomas (61.5%) and in a significant proporti

55 gnetic resonance imaging, which uncovered an ovarian carcinoma, a follicular lymphoma, and a Hodgkin

56 Analogous to mesothelioma and ovarian carcinoma, a significant increase of MSLN was de

57 h a markedly different integrin fingerprint: ovarian carcinoma A2780 (almost no alpha(v)beta(3), mode

58 All compounds are active in both human ovarian carcinoma A2780 cells and cisplatin-resistant A2

59 In vitro studies on human ovarian carcinoma A2780 cells were carried out to invest

60 0 kDa) were determined in mice bearing human ovarian carcinoma A2780 xenografts.

61 mined micrometastases from a murine model of ovarian carcinoma after injection of a radioimmunoconjug

62 pressor, as a gene associated with recurrent ovarian carcinomas after chemotherapy.

63 We report that recurrent ovarian carcinomas after paclitaxel/carboplatin treatmen

64 hown to deliver siRNA to disseminated murine ovarian carcinoma allograft tumors following intraperito

65 gfA tumors, an aggressive xenograft model of ovarian carcinoma, also conferring a survival benefit in

66 In this study, we focused on ovarian carcinoma and analyzed gene expression levels us

67 dl922-947 has potency in ovarian carcinoma and i.p. delivery in icodextrin may en

68 t p53 signatures and STICs are precursors of ovarian carcinoma and identify a window of 7 years betwe

69 that SOX2 associates with stem cell state in ovarian carcinoma and induction of SOX2 imposes CSC prop

70 hat Jagged-1 is the primary Notch3 ligand in ovarian carcinoma and Jagged-1/Notch3 interaction consti

71 minal helicase 1 (BRIP1) are associated with ovarian carcinoma and may also contribute to breast canc

72 , we show that in human and mouse epithelial ovarian carcinoma and mouse lung carcinoma, the interact

73 tion between MDSCs and CSCs in patients with ovarian carcinoma and showed that MDSCs inhibited T cell

74 ial therapeutic target in a subset of serous ovarian carcinoma and stromal sarcoma patients.

75 xpression is an adverse prognostic factor in ovarian carcinoma and TG2 targeting may be an attractive

76 indings shed new light into understanding of ovarian carcinomas and may provide a new therapeutic str

77 pression of WNT7A and FGF1 are correlated in ovarian carcinomas and poor overall patient survival.

78 pitope is selectively generated within human ovarian carcinomas and this collagen epitope plays a rol

79 mpound 15: IC50 0.025 and 0.33 nM, in A2780 (ovarian carcinoma) and MCF-7 (breast), respectively) and

80 HT-29 (human colon carcinoma), A2780 (human ovarian carcinoma), and A2780cis (cisplatin-resistant hu

81 ons, >30% had no family history of breast or ovarian carcinoma, and >35% were 60 y or older at diagno

82 d in the plasma and ascites of patients with ovarian carcinoma, and VEGFR3 expression was found in th

83 onchoalveolar, small cell lung, thyroid, and ovarian carcinomas, and chondrosarcoma, respectively.

84 is expressed in a significant proportion of ovarian carcinomas, and in the CAOV3 and SKOV3 ovarian c

85 Immunocompetent models of ovarian carcinoma are required for further evaluation of

86 b and other novel agents in the treatment of ovarian carcinoma are summarized.

87 of MDSCs and their interaction with CSCs in ovarian carcinoma are unclear.

88 Ovarian carcinomas are a heterogeneous group of neoplasm

89 owth and spread of malignant tumors, such as ovarian carcinomas, are governed in part by complex inte

90 type 2 (HER2) is overexpressed in breast and ovarian carcinoma, as well as in other malignancies, HER

91 There were 64 primary and 46 recurrent ovarian carcinomas assessed.

92 Ovarian carcinoma-associated mesenchymal stem cells (CA-

93 In ovarian carcinoma-bearing mice, this induced T cell-medi

94 Three main groups of samples (epithelial ovarian carcinoma, borderline ovarian tumours, normal ov

95 d integIRTy to three public cancer datasets (ovarian carcinoma, breast cancer, glioblastoma) for cros

96 ion and activation occur most prevalently in ovarian carcinoma but were also detected in four other m

97 ncreased RSPO1 expression is associated with ovarian carcinomas, but it is not clear whether it is a

98 d other tumor suppressor genes predispose to ovarian carcinomas, but the overall burden of disease du

99 x E3 ligase, suppresses tumor progression in ovarian carcinomas by inhibiting aerobic glycolysis.

100 More patients with ovarian carcinoma carry cancer-predisposing mutations an

101 lyse germline and somatic alterations in 429 ovarian carcinoma cases and 557 controls.

102 s (EECs), the likely precursor of clear cell ovarian carcinomas (CCOCs).

103 were evaluated in BALB/C nu/nu mice bearing ovarian carcinoma cell (SKOV-3) xenografts.

104 proapoptotic functions, SPARC also abrogates ovarian carcinoma cell adhesion, a key step in peritonea

105 no loss of activity in the resistant A2780AD ovarian carcinoma cell line known to overexpress the ABC

106 Combinatorial mutations in the human ES2 ovarian carcinoma cell line were also assessed with TRAC

107 the 3+ cancer stem cell markers in the human ovarian carcinoma cell line, OVCAR-5, and is also highly

108 ty to block the migration of a highly motile ovarian carcinoma cell line, SKOV-3, by using a 384-well

109 e methods and MixMHCpred on new data from an ovarian carcinoma cell line.

110 lopmental regulator Six1 is overexpressed in ovarian carcinoma cell lines (OCC) compared with normal

111 cytotoxicity for the protected compounds in ovarian carcinoma cell lines sensitive and resistant to

112 Overexpression of IHPK2 sensitized ovarian carcinoma cell lines to the growth-suppressive a

113 Mouse serous and endometrioid ovarian carcinoma cell lines were tested in vitro agains

114 Ovarian carcinoma cell lines were used to evaluate the e

115 mammary epithelial cells, and in breast and ovarian carcinoma cell lines, represses IFN-stimulated g

116 totoxicity and cell uptake data in two human ovarian carcinoma cell lines.

117 ed inhibition of AURKA significantly reduced ovarian carcinoma cell migration and adhesion and the ac

118 genetic and epigenetic changes that lead to ovarian carcinoma cell transformation.

119 ma), and A2780cis (cisplatin-resistant human ovarian carcinoma) cell lines, with selected complexes'

120 ompounds were active against COX-1 in intact ovarian carcinoma cells (OVCAR-3).

121 sts were either mixed with fluorescent human ovarian carcinoma cells before subcutaneous implantation

122 BRCA1-deficient ovarian carcinoma cells exhibit hypermethylation within

123 blasts expressing endogenous Pyk2 and in ID8 ovarian carcinoma cells expressing both Pyk2 and FAK.

124 extent of DNA adduct formation in the A2780 ovarian carcinoma cells for four osmium(II) arene comple

125 tural retinoid, arrests the growth of CA-OV3 ovarian carcinoma cells in G(0)-G(1).

126 ATRA) has been shown to arrest the growth of ovarian carcinoma cells in G0/G1 and to significantly el

127 human ovarian epithelial cells in vitro and ovarian carcinoma cells in vivo.

128 Expression of MSX2 in selected ovarian carcinoma cells induced changes suggestive of ep

129 t released from virally infected human CAOV2 ovarian carcinoma cells inhibited peritoneal disseminati

130 A2780 human ovarian carcinoma cells showed high levels of EpoR expre

131 assay to evaluate their ability to sensitize ovarian carcinoma cells to Bcl-xL-targeting strategies.

132 During initial tumorigenesis, ovarian carcinoma cells undergo an epithelial-to-mesench

133 Treatment of human ovarian carcinoma cells with 50 muM 6F-GalNAc (Ac3) inhi

134 ainst syngeneic Lewis lung carcinoma and ID8 ovarian carcinoma cells, a defect that in the ID8 model

135 olar) binding affinity towards HER2-positive ovarian carcinoma cells, but higher-valence conjugates i

136 secretion of several angiogenic factors from ovarian carcinoma cells, most prominently interleukin (I

137 tion of cell survival and PDK1 expression in ovarian carcinoma cells, suggesting a unique function fo

138 of ChIP-Seq and microarray studies in human ovarian carcinoma cells, we show that the two zinc finge

139 association between PITX2 and Wnt pathway in ovarian carcinoma cells.

140 and cisplatin-resistant A2780 and A2780cisR ovarian carcinoma cells.

141 cisplatin resistance to cultured high-grade ovarian carcinoma cells.

142 enograft models involving SKOV3ip1 and HeyA8 ovarian carcinoma cells.

143 the cisplatin-induced transcription in human ovarian carcinoma cells.

144 mor growth independent of Epo in A2780 human ovarian carcinoma cells.

145 MDA-7/IL-24 inhibits cell survival of human ovarian carcinoma cells.

146 xpression of IL-6 mRNA and protein levels in ovarian carcinoma cells.

147 c were also down-regulated in p53-null human ovarian carcinoma cells.

148 and (18)F-FES for ER was evaluated in SKOV3 ovarian carcinoma cells.

149 ated Perp in ErbB2-positive human breast and ovarian carcinoma cells.

150 o ferroptosis sensitivity in human renal and ovarian carcinoma cells.

151 Cytotoxicity assays on human epithelial ovarian carcinoma cisplatin-sensitive and -resistant cel

152 High-grade serous ovarian carcinoma commonly arises from fallopian tube se

153 y 30% of RAD001-treated mice developed early ovarian carcinoma confined within the ovary, whereas all

154 uced mouse mammary adenocarcinomas and human ovarian carcinomas confirmed the activity of the pathway

155 Ovarian carcinoma could originate from any of three pote

156 1B (PTP1B) was underexpressed in a panel of ovarian carcinoma-derived cell lines, compared with immo

157 sis in normal ovarian function as well as in ovarian carcinoma development and disease progression.

158 The biology of ovarian carcinoma differs from that of hematogenously me

159 Endometrioid ovarian carcinoma (EnOC) demonstrates substantial clinic

160 patients with platinum-resistant epithelial ovarian carcinoma (EOC) or peritoneal serous carcinoma (

161 rates for patients with advanced epithelial ovarian carcinoma (EOC) remain disappointing, and the de

162 i.p. metastatic dissemination of epithelial ovarian carcinoma (EOC).

163 utcome of high-grade serous (HGS) epithelial ovarian carcinomas (EOC), we evaluated the association b

164 ransferase GnT-III is elevated in epithelial ovarian carcinomas (EOCs) and leads to the production of

165 luation of patients with suspected recurrent ovarian carcinoma, especially when CA-125 levels are ris

166 % of the late-stage (stages II, III, and IV) ovarian carcinomas examined, with late-stage carcinomas

167 isplatin, and patients with BRCA1-associated ovarian carcinomas experience improved outcomes with pla

168 also differentially regulated in late-stage ovarian carcinomas, further confirming the importance of

169 ibitor, has anticancer activity in recurrent ovarian carcinoma harbouring a BRCA mutation or high per

170 therapy to date in the setting of epithelial ovarian carcinoma has come from angiogenesis inhibition.

171 Mouse models of ovarian carcinoma have been developed that recapitulate

172 gulation of endogenous iPLA(2) expression in ovarian carcinoma HEY cells results in decreased migrati

173 high risk of recurrence in high-grade serous ovarian carcinoma (HGS-OvCa), the development of outcome

174 High-grade serous ovarian carcinoma (HGSC), the most common subtype of ova

175 on in the heterogeneity of high-grade serous ovarian carcinoma (HGSC), we perform mass spectrometry-b

176 High-grade serous ovarian carcinoma (HGSOC) and basal-like breast cancer (

177 High-grade serous ovarian carcinoma (HGSOC) is a lethal disease for which

178 A key feature of high-grade serous ovarian carcinoma (HGSOC) is frequent amplification of t

179 High-grade serous ovarian carcinoma (HGSOC) is the most common and aggress

180 High-grade serous ovarian carcinoma (HGSOC) is the most frequent type of o

181 High-grade serous ovarian carcinoma (HGSOC) is the most lethal gynecologic

182 High-grade serous ovarian carcinoma (HGSOC) is the most lethal gynecologic

183 The cell-of-origin of high grade serous ovarian carcinoma (HGSOC) remains controversial, with fa

184 transcriptome subtypes of high-grade serous ovarian carcinoma (HGSOC), but their interpretation and

185 High-grade serous ovarian carcinoma (HGSOC), the most lethal gynecological

186 are a defining feature of high-grade serous ovarian carcinoma (HGSOC).

187 ively, for the majority of high-grade serous ovarian carcinomas (HGSOC) provide the necessary context

188 in organoids derived from high-grade serous ovarian carcinomas (HGSOC), an aggressive cancer charact

189 neal fluid from women with high-grade serous ovarian carcinomas (HGSOCs).

190 cinoma: HR = 0.74 [0.59-0.93], p = 0.01, and ovarian carcinoma: HR = 0.80 [0.70-0.93], p = 0.003.

191 lysis of data from an independent set of 253 ovarian carcinomas in The Cancer Genome Atlas showed tha

192 While CHIP is downregulated in ovarian carcinoma, induced expression of CHIP results in

193 rily metastatic within the abdominal cavity, ovarian carcinomas initially spread to adjacent organs b

194 independent cohort of 226 high-grade serous ovarian carcinomas into groups of high risk and low risk

195 ans and are only temporarily chemosensitive, ovarian carcinoma is a deadly disease, with a cure rate

196 High-grade serous ovarian carcinoma is characterised by TP53 mutation and

197 1024delT [p.Tyr342Thrfs*30]) associated with ovarian carcinoma is located between the regions encodin

198 Ovarian carcinoma is the fifth common cause of cancer de

199 Epithelial ovarian carcinoma is the most common cause of death from

200 Serous ovarian carcinoma is the most lethal gynecological malig

201 For small-cell ovarian carcinomas, it is important to differentiate tho

202 Although current clinical management of ovarian carcinoma largely fails to take this heterogenei

203 Low-grade serous ovarian carcinomas (LGSC) are associated with a poor res

204 Low-grade serous ovarian carcinomas (LGSOCs) have historically low chemot

205 growing evidence that most high-grade serous ovarian carcinomas likely arise from local dissemination

206 Six1 knockdown in the TRAIL-resistant SKOV3 ovarian carcinoma line dramatically sensitizes the cells

207 both cisplatin sensitive and resistant human ovarian carcinoma lines the dinuclear complexes show enh

208 immunotherapy of solid tumors, in particular ovarian carcinoma, may be improved by the use of IgE Abs

209 metastatic pancreatic adenocarcinoma, OvCar3 ovarian carcinoma, MDA-MB-231 breast adenocarcinoma, and

210 most abundant leukocyte subset in the solid ovarian carcinoma microenvironment) from an immunosuppre

211 Here, we show that, in the ovarian carcinoma microenvironment, CD11c(+)MHC-II(+) de

212 ive CD11c(+) antigen-presenting cells in the ovarian carcinoma microenvironment.

213 Mucinous ovarian carcinoma (MOC) is a unique subtype of ovarian c

214 the epithelium stresses the UPS and renders ovarian carcinoma more sensitive to apoptosis in respons

215 ted peritoneal neutrophil infiltration in an ovarian carcinoma mouse model.

216 In cohorts of primary ovarian carcinomas, mTORC1 and UPR signaling pathways we

217 Women with nonmucinous ovarian carcinoma (n = 1,001) enrolled onto a population

218 melanoma (A375), renal carcinoma (ACHN), and ovarian carcinoma (NIH-OVCAR-3) cells were treated with

219 These mutations were detectable only in ovarian carcinomas of women whom have had previous chemo

220 Ovarian carcinoma (OvC) remains a major therapeutic chal

221 A dualistic pathway model of ovarian carcinoma (OvCA) pathogenesis has been proposed:

222 major barrier to successful immunotherapy in ovarian carcinomas (OvCa).

223 In ovarian cancer, 84 (75%) of 112 ovarian carcinomas overexpressed LINE-1.

224 olon carcinoma, melanoma, hepatic carcinoma, ovarian carcinoma, pancreatic cancer, and renal cell car

225 (CCC) is one of the most malignant types of ovarian carcinomas, particularly at advanced stages.

226 t CXCR3(+) Treg are highly enriched in human ovarian carcinomas, particularly in solid tumor masses,

227 erexpression as an important factor in human ovarian carcinoma pathogenesis.

228 erexpression as an important factor in human ovarian carcinoma pathogenesis.Oncogene advance online p

229 who received xenografts and includes (1) an ovarian carcinoma patient receiving three intraperitonea

230 of this sequential immunotherapy to advanced ovarian carcinoma patients also revealed that tumor dest

231 y of liposomes from the blood circulation of ovarian carcinoma patients.

232 High-grade serous ovarian carcinoma presents significant clinical and ther

233 ate elevated GC UNC-45 protein expression in ovarian carcinoma proliferation and metastasis.

234 g reverse-phase protein arrays, we generated ovarian carcinoma protein expression profiles on 412 cas

235 In pathological angiogenesis of human ovarian carcinomas, reduced VEC expression paralleled de

236 red to all women diagnosed with nonmucinous, ovarian carcinoma, regardless of family history.

237 ography (CT) scans in patients with advanced ovarian carcinoma reported to have undergone optimal pri

238 nd 57% of STICs, with and without concurrent ovarian carcinomas, respectively, exhibited intense LINE

239 Until fairly recently, high-grade serous ovarian carcinoma seemed to be one of the only known dev

240 Ovarian carcinoma serum samples are used for the detecti

241 ll viability, proliferation and migration of ovarian carcinoma (SKOV-3) and prostate carcinoma (PC-3)

242 In EGCG-treated human ovarian carcinoma SKOV3 cells, decreased levels of sever

243 Additionally, incubation of human ovarian carcinoma (SKOV3) cells with an NDBF-caged versi

244 We report that in human serous ovarian carcinoma (SOC) cells, SOX2 expression increases

245 Recent studies suggest that some serous ovarian carcinomas (SOCs) arise from the fallopian tube

246 documented in several tumor types including ovarian carcinoma, suggesting an involvement of SOX2 in

247 in the ascites of a cohort of patients with ovarian carcinoma, suggesting their possible induction/e

248 but particularly in recurrent chemoresistant ovarian carcinomas, suggesting a biological role for NAC

249 TNS4 expression in human colon carcinoma and ovarian carcinoma suggests TNS4 plays a critical role in

250 tions to those observed in high-grade serous ovarian carcinomas suggests that genetic biomarkers iden

251 In human ovarian carcinomas, TAM infiltration and CCR2 expression

252 tegies under investigation for patients with ovarian carcinoma that illustrate many of these issues.

253 inducible p53-dependent model of aggressive ovarian carcinoma that recapitulates the leukocyte infil

254 clinical samples of BRCA1-mutated recurrent ovarian carcinomas that have developed resistance to pla

255 have been elucidated as driver mutations in ovarian carcinomas that transform into an invasive pheno

256 tumors that resemble human metastatic serous ovarian carcinoma, the most common type of ovarian cance

257 e origin and initiation of high-grade serous ovarian carcinomas, the most common and deadliest ovaria

258 lines, and Rsf-1 immunoreactivity in primary ovarian carcinoma tissues correlated with in vitro pacli

259 Epithelial ovarian carcinoma tissues express high levels of tumor n

260 we used drug-resistant spheroid cultures of ovarian carcinoma to evaluate the uptake and cytotoxicit

261 and recurrence outcomes in the treatment of ovarian carcinoma to identify signature genes that can m

262 croRNA (miR) expression in serous epithelial ovarian carcinomas to assess the possibility of a miR si

263 sessed primary and recurrent BRCA1/2-mutated ovarian carcinomas to define the frequency of secondary

264 CA wild-type and LOH high platinum-sensitive ovarian carcinomas treated with rucaparib, progression-f

265 CA wild-type and LOH high platinum-sensitive ovarian carcinomas treated with rucaparib, progression-f

266 tivity in the CAM model and in a xenografted ovarian carcinoma tumor (A2780) grown on the CAM.

267 clinical outcomes with regard to epithelial ovarian carcinoma tumor methylation to date.

268 TE to analyze exome sequencing data from 214 ovarian carcinoma tumor-normal pairs.

269 for Nectin-4, ADAM10, and ADAM17 in primary ovarian carcinoma tumors, secondary omental metastases,

270 and cystadenomas, whereas its expression in ovarian carcinomas was strongly associated with high tum

271 didate oncogenic driver in high-grade serous ovarian carcinoma, we evaluated the functional role of c

272 In ovarian carcinoma, we previously demonstrated that Bcl-x

273 way are currently in clinical trials against ovarian carcinoma, we screened normal ovarian and carcin

274 th recurrent, platinum-sensitive, high-grade ovarian carcinoma were classified into one of three pred

275 luable patients suspected of having advanced ovarian carcinoma were enrolled in a prospective protoco

276 Patients with platinum-sensitive, recurrent ovarian carcinoma were randomly assigned to rucaparib (6

277 rs from patients whose primary BRCA2-mutated ovarian carcinomas were treated with cisplatin.

278 many carcinomas, including high-grade serous ovarian carcinoma, where it contributes to genomic insta

279 rentiation and apoptosis is overexpressed in ovarian carcinomas, where it modulates epithelial-to-mes

280 st important risk factor for sporadic serous ovarian carcinoma, whereas a germ-line mutation in BRCA1

281 cancers (HGSEMC), otherwise referred to as 'ovarian carcinomas', which frequently develop from fimbr

282 The most common ovarian cancer is epithelial ovarian carcinoma, which is characterised by few early s

283 ines, MCF-7 breast adenocarcinoma and SKOV-3 ovarian carcinoma, while the uptake of the shielded mice

284 s) with histopathologically proven recurrent ovarian carcinoma who underwent CE CT and PET/CT before

285 DK12 is a recurrently mutated gene in serous ovarian carcinoma, whose downregulation is associated wi

286 CA2 mutation [5193C>G (Y1655X)] carrier with ovarian carcinoma with acquired cisplatin resistance and

287 otherapy in patients with platinum-resistant ovarian carcinoma with low tumor human epidermal growth

288 le structures and developed low-grade serous ovarian carcinomas with 100% penetrance within 18 weeks.

289 olymerase (PARP) inhibitors have activity in ovarian carcinomas with homologous recombination deficie

290 Although ovarian carcinomas with mutated BRCA1 or BRCA2 are sensi

291 Ovarian carcinomas with mutations in the tumour suppress

292 ween development of a STIC and initiation of ovarian carcinoma, with metastases following rapidly the

293 ioavailable and displays efficacy in a human ovarian carcinoma xenograft model.

294 In human ovarian carcinoma xenograft models, high levels of solub

295 extracellular matrix in two orthotopic human ovarian carcinoma xenograft models.

296 Targeting of HER2-overexpressing SKOV-3 ovarian carcinoma xenografts in nude mice was studied fo

297 ce imaging to quantify the response of human ovarian carcinoma xenografts to dl922-947.

298 r-gemcitabine conjugates against A2780 human ovarian carcinoma xenografts.

299 ng experiments against the IGROV-1/Pt1 human ovarian carcinoma xenotransplanted in nude mice, compoun

300 In primary ovarian carcinomas, ZEB1 binding site methylation and TA