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 abeled antibody administered in vivo against ovarian carcinoma.

3 relapsed peritoneal metastasis in epithelial ovarian carcinoma.

4 tional relevance of SOX2 expression in human ovarian carcinoma.

5 presented among miRNA genes overexpressed in ovarian carcinoma.

6 responsible for altered miRNA expression in ovarian carcinoma.

7 were not previously implicated in inherited ovarian carcinoma.

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

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

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

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

12 olonized by advanced and relapsed metastatic ovarian carcinoma.

13 -associated macrophages in 103 patients with ovarian carcinoma.

14 hensive review of the surgical management of ovarian carcinoma.

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

16 offers an attractive therapeutic approach in ovarian carcinoma.

17 all placebo-treated mice developed advanced ovarian carcinoma.

18 ethod to inhibit peritoneal dissemination of ovarian carcinoma.

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

20 MKK4) as a metastasis suppressor protein in ovarian carcinoma.

21 that B7-H4 is a promising new biomarker for ovarian carcinoma.

22 SF767 human glioblastoma and the SKOV3 human ovarian carcinoma.

23 iogenesis observed during the progression of ovarian carcinoma.

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

25 h CDK12 inactivation in patients with serous ovarian carcinoma.

26 regression in the treatment of mice bearing ovarian carcinoma.

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

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

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

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

31 broader clinical utility in ERalpha-positive ovarian carcinoma.

32 patients with platinum-resistant/refractory ovarian carcinoma.

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

34 the leading causes of therapeutic failure in ovarian carcinomas.

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

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

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

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

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

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

41 n transgenic mice that spontaneously develop ovarian carcinomas.

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

43 urprisingly ineffective against SKOV-3 human ovarian carcinomas.

44 can be a potential therapeutic approach for ovarian carcinomas.

45 hibits aberrant patterns in subsets of human ovarian carcinomas.

46 versely correlated with PKM2 levels in human ovarian carcinomas.

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

48 8 tumors were characteristic of human serous ovarian carcinomas.

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

50 XO3a in a vast majority of high-grade serous 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 Human ovarian carcinoma 2008 cells were transfected with an hR

55 levels in 98 women with invasive epithelial ovarian carcinoma, 30 with low malignant potential (LMP)

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

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

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

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

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

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

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

76 rcinomas but was negligible in both mucinous ovarian carcinomas and normal ovary.

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 ptides presented on the surface of melanoma, ovarian carcinoma, and B lymphoblastoid cells, we find 5

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

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

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

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

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

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

89 Ovarian carcinomas are a heterogeneous group of neoplasm

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

91 EYA2 was amplified in 14.8% of ovarian carcinomas, as detected by array-based comparati

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

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 nd PKCiota overexpression was seen mostly in ovarian carcinoma but not in other solid tumors.

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

98 cation of this region in 13.2% of high-grade ovarian carcinomas but not in any of low-grade carcinoma

99 n was positive in approximately 89% of human ovarian carcinomas but was negligible in both mucinous o

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

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

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

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

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

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

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

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

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

109 The ovarian carcinoma cell line MA148 was genetically modifi

110 A cisplatin-resistant ovarian carcinoma cell line PE01CDDP was derived from th

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

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

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

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

115 We find that ovarian carcinoma cell lines exhibit greater sensitivity

116 ighly cytotoxic to PA-1, IGROV-1, and SK-OV3 ovarian carcinoma cell lines in vitro.

117 ues relative to benign ovarian tumors and in ovarian carcinoma cell lines relative to immortalized su

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

119 Most human ovarian carcinoma cell lines tested secreted significant

120 fficacy than Ad5 WT, dl309, or dl1520 in all ovarian carcinoma cell lines tested, which was associate

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

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

123 Ovarian carcinoma cell lines were transfected in vitro w

124 Ovarian carcinoma cell lines were used to evaluate the e

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

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

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

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

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

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

131 ghts the role of unique interactions between ovarian carcinoma cells and interstitial collagens in th

132 at DDP triggers the rapid loss of hCTR1 from ovarian carcinoma cells at clinically relevant concentra

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

134 BRCA1-deficient ovarian carcinoma cells exhibit hypermethylation within

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

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

137 ter tumor burden and more invasive growth of ovarian carcinoma cells in an orthotopic mouse model.

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

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

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

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

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

143 Ovarian carcinoma cells preferentially adhere to interst

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

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

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

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

148 Treatment of colon and ovarian carcinoma cells with the anticancer genotoxic ag

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

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

151 In ATRA-treated ovarian carcinoma cells, PP2A binds to Rb2/p130 and deph

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

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

154 KT and FAS, we used SKOV3, C200, and OVCAR10 ovarian carcinoma cells, which have constitutively activ

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

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

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

158 enograft models involving SKOV3ip1 and HeyA8 ovarian carcinoma cells.

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

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

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

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

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

164 nic potential of the HER2/neu-overexpressing ovarian carcinoma cells.

165 down-regulation of hCTR1 expression in human ovarian carcinoma cells.

166 HeLa cervical carcinoma cells and A2780-SCA ovarian carcinoma cells.

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

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

169 We investigated the efficacy of dl922-947 in ovarian carcinoma; compared its activity to wild-type ad

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

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

172 Ovarian carcinoma could originate from any of three pote

173 1B (PTP1B) was underexpressed in a panel of ovarian carcinoma-derived cell lines, compared with immo

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

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

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

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

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

179 ed in gene expression profiles of epithelial ovarian carcinomas (EOC) is the gene for human epididymi

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

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

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

183 % of the late-stage (stages II, III, and IV) ovarian carcinomas examined, with late-stage carcinomas

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

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

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

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

188 Mouse models of ovarian carcinoma have been developed that recapitulate

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 1024delT [p.Tyr342Thrfs*30]) associated with ovarian carcinoma is located between the regions encodin

206 Ovarian carcinoma is the fifth common cause of cancer de

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

208 Serous ovarian carcinoma is the most lethal gynecological malig

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

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

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

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

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

214 Herein, we show that ovarian carcinoma manifests an overstressed UPS by compa

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

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

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

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

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

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

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

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

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

224 We randomly assigned patients with stage III ovarian carcinoma or primary peritoneal carcinoma with n

225 , raised the possibility of lung, breast, or ovarian carcinoma or thymoma.

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

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

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

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

230 Ovarian carcinomas, particularly recurrent forms, are fr

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

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

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

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

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

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

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

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

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

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

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

242 Ovarian carcinoma serum samples are used for the detecti

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

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

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

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

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

248 , low-grade, and high-grade papillary serous ovarian carcinomas suggest that LMP tumors are distinct

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

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

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

252 nes have only been reported in a minority of ovarian carcinomas, suggesting that alterations in TGF-b

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

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

255 In human ovarian carcinomas, TAM infiltration and CCR2 expression

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

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

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

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

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

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

262 are evident in both low-grade and high-grade ovarian carcinoma tissues relative to benign ovarian tum

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 me inhibitor PS-341 slows the growth of ES-2 ovarian carcinoma xenograft in immunodeficient mice.

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

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

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