ライフサイエンスコーパス: ovarian tumor

1 obably by regulating alternative splicing of ovarian tumor.

2 and its expression is markedly increased in ovarian tumors.

3 rs but in only 0.4% (2/485) of other primary ovarian tumors.

4 creased in the serum of women with malignant ovarian tumors.

5 nding protein-2 (CtBP2) is elevated in human ovarian tumors.

6 g female nu/nu mice bearing orthotopic A2780 ovarian tumors.

7 of peritoneal organs, particularly colon and ovarian tumors.

8 nomic relationship between these subtypes of ovarian tumors.

9 domain of DICER1 are common in nonepithelial ovarian tumors.

10 an cancers and expressed at higher levels in ovarian tumors.

11 ay be an innovative therapeutic strategy for ovarian tumors.

12 cancer stem cells (CSCs) in both breast and ovarian tumors.

13 aining in peritoneal xenografts and in human ovarian tumors.

14 ermethylation in DNA derived from breast and ovarian tumors.

15 tion protein that is overexpressed in 90% of ovarian tumors.

16 Two patients had ovarian tumors.

17 er-associated islands in a set of breast and ovarian tumors.

18 ted deregulation of PELP1/MNAR expression in ovarian tumors.

19 iate resistance to platinum in BRCA1-mutated ovarian tumors.

20 he development and maintenance of epithelial ovarian tumors.

21 n of the general cell (GC) UNC-45 isoform in ovarian tumors.

22 deficiency is exploited to treat breast and ovarian tumors.

23 ading domain mutations in three endometrioid ovarian tumors.

24 RCA2 germline mutation-associated breast and ovarian tumors.

25 rious ovarian defects, ranging from cysts to ovarian tumors.

26 y be important particularly in rapidly fatal ovarian tumors.

27 e of PD-1 in TIDCs derived from mice bearing ovarian tumors.

28 platinum-resistant ovarian tumors vs primary ovarian tumors.

29 domain were found in 30 of 102 nonepithelial ovarian tumors (29%), predominantly in Sertoli-Leydig ce

30 (1) and high risk (2) ovarian stroma, benign ovarian tumors (3), low grade (4) and high grade (5) ser

31 alyses of 102 non-small cell lung tumors, 61 ovarian tumors, 70 liver tumors, 156 glioblastoma multif

32 ations were demonstrated in 10 of 110 type I ovarian tumors (9.1%) including low-grade serous, low-gr

33 promoted tumor progression by modulating the ovarian tumor aggressiveness and microenvironment.

34 FRalpha), which is expressed widely on human ovarian tumors, along with a syngeneic rat tumor model e

35 opean-based, algorithmic-style International Ovarian Tumor Analysis (IOTA) Assessment of Different Ne

36 rnational, prospective, cohort International Ovarian Tumor Analysis Phase 5 (IOTA5) study, patients a

37 We previously showed that ovarian tumor and associated macrophages expressed B7-H4

38 erline tumor), one patient had an androgenic ovarian tumor and two patients had hyperreactio luteinal

39 aging showed regression of established HeyA8 ovarian tumors and [18F]FDG PET with MR showed rapid dec

40 is found to be overexpressed in a subset of ovarian tumors and cancer cell lines.

41 we show that FTO expression is suppressed in ovarian tumors and cancer stem cells (CSC).

42 ing expression of miRNAs and mRNAs in serous ovarian tumors and cell lines and normal ovarian surface

43 All human ovarian tumors and cell lines displayed ALDH activity.

44 ment in cancer from additional 28 non-serous ovarian tumors and compared our results to TCGA ovarian

45 The dissemination of ovarian tumors and growth as spheroids accompanies late-

46 The MUC4 mucin is overexpressed in ovarian tumors and has a role in the invasiveness of OC

47 equenced this region of DICER1 in additional ovarian tumors and in certain other tumors and queried t

48 ng enzyme, is significantly overexpressed in ovarian tumors and its expression increases in response

49 ype Bap1 allele was lost in both spontaneous ovarian tumors and mesotheliomas, resulting in the loss

50 east approximately 36% of miRNAs in advanced ovarian tumors and miRNA down-regulation contributes to

51 transcriptomes or exomes of 14 nonepithelial ovarian tumors and noted closely clustered mutations in

52 n, and E-cadherin were investigated in human ovarian tumors and paired peritoneal metastases wherein

53 d epithelial components of high-grade serous ovarian tumors and TGF-beta-treated normal ovarian fibro

54 tivation of RSPO1 is sufficient in promoting ovarian tumors and thus supports a direct involvement of

55 ells require to induce host immunity against ovarian tumors and which of the host immune cells are in

56 es, including benign and borderline mucinous ovarian tumors, and compare these to tumors from other p

57 in omental metastases as compared to primary ovarian tumors, and FABP4 expression was detected in ova

58 sed these cell lines to establish orthotopic ovarian tumors, and found that inducible expression of a

59 MNAR is 2- to 3-fold overexpressed in 60% of ovarian tumors, and PELP1/MNAR deregulation occurs in al

60 ecific to CAFs in advanced high-grade serous ovarian tumors, and showed how TGF-beta stimulates ovari

61 implement these methods on a small number of ovarian tumors, and the results suggest possible differe

62 e from human cancer cell lines and the human ovarian tumor array data sets, documented significant ov

63 expression were decreased in malignant human ovarian tumors as well as human ovarian cancer cell line

64 rs, borderline/low malignant potential (LMP) ovarian tumors as well as invasive EOC and the other con

65 the tolerogenic phenotype of human and mouse ovarian tumor-associated DCs.

66 Additionally, non-small cell lung and ovarian tumor AUC was at least twice that of cisplatin i

67 on-invasive summary-statistic of the primary ovarian tumor based on 4 descriptors, which we name "Rad

68 We also describe a subclassification of ovarian tumors based on CBX7 and TWIST-1 expression, whi

69 NETs were detected in the omentum of ovarian tumor-bearing mice before metastasis and of wome

70 and PD-1-PD-L1 pathways prolongs survival of ovarian tumor-bearing mice by prevention of immunosuppre

71 siRNA-mediated LPP silencing in ovarian tumor-bearing mice improved paclitaxel delivery

72 of the resultant FA-3DNA-siHuR conjugates to ovarian tumor-bearing mice suppressed tumor growth and a

73 y disease, we conducted preclinical tests in ovarian tumor-bearing mice to evaluate the therapeutic e

74 Similarly, treatment of ovarian tumor-bearing mice with PD-1 blocking antibody r

75 eal administration of (166)Ho-MSNs to SKOV-3 ovarian tumor-bearing mice.

76 ignaling in both murine xenografts and human ovarian tumor biopsies.

77 ed tissue microarrays, one containing benign ovarian tumors, borderline/low malignant potential (LMP)

78 Dissimilarly, serous borderline ovarian tumors (BOT) can progress into low-grade serous

79 In NFATc1-induced skin and ovarian tumors, both cells with NFATc1 activation and ne

80 essed in metastases and advanced-stage human ovarian tumors but not in normal ovarian epithelium.

81 B and SRp20 is associated with malignancy of ovarian tumors but not with stage of invasive EOC.

82 have a 3-5-fold higher incidence specific to ovarian tumors, but not lymphoma, when compared with the

83 tate tumors, non-small cell lung tumors, and ovarian tumors, but not nontumor prostate or liver tissu

84 expression in a tissue microarray of serous ovarian tumors by immunohistochemistry and found that 88

85 This suggests clinical potential to localize ovarian tumors by MR for staging and surgical planning,

86 lls to promote the regression of established ovarian tumors by over one order of magnitude.

87 -derived xenografts to demonstrate that most ovarian tumors can be matched to effective biomarker-gui

88 Wnt5a promoted ovarian tumor cell adhesion to peritoneal mesothelial ce

89 ent effector cells in MOv18 IgE Ab-dependent ovarian tumor cell cytotoxicity in vitro.

90 In this study, we demonstrate that ovarian tumor cell debris generated by first-line platin

91 that overexpression of SRp20 is required for ovarian tumor cell growth and survival.

92 C) and knockdown of PTB expression inhibited ovarian tumor cell growth and transformation properties.

93 hat CD73 and extracellular adenosine enhance ovarian tumor cell growth as well as expression of antia

94 Monocytes mediated MOv18 IgE-dependent ovarian tumor cell killing in vitro by two distinct path

95 GA protein and mRNA levels were decreased in ovarian tumor cell lines not expressing the protein p53.

96 One mechanism of YPEL3 downregulation in ovarian tumor cell lines seems to be hypermethylation of

97 Furthermore, lung and ovarian tumor cell lines that retain RASSF1A expression

98 We identified ovarian tumor cell lines that retain UBB in a repressed

99 In cell culture, ovarian tumor cell spheroids can exhibit elevated resist

100 apoptotic pathways, culminating in decreased ovarian tumor cell survival.

101 erize a self-renewing subpopulation of human ovarian tumor cells (ovarian cancer-initiating cells, OC

102 n breast tumor cells (MCF-7 cells) and human ovarian tumor cells (SK-OV-3.ipl cells).

103 hyaluronan synthase (HAS) activity in human ovarian tumor cells (SK-OV-3.ipl cells).

104 rthermore, high levels of CD73 expression in ovarian tumor cells abolished the good prognosis associa

105 nsequences of ascites-induced compression on ovarian tumor cells and components of the peritoneal mic

106 -Np bind with high specificity to both human ovarian tumor cells and tumor endothelial cells in vitro

107 dentified a set of key cytokines secreted by ovarian tumor cells and tumor-associated APCs that favor

108 RNAi-mediated silencing of Dll4 in ovarian tumor cells and tumor-associated endothelial cel

109 , a stem cell regulatory factor expressed in ovarian tumor cells and vasculature, regulates ALDH(+) o

110 d-1 as the highest expressed Notch ligand in ovarian tumor cells as well as in peritoneal mesothelial

111 e chemotherapy resistance in some breast and ovarian tumor cells displaying stem cell marker properti

112 ide that selectively binds integrin beta3 on ovarian tumor cells enhances the phosphorylation of the

113 sent study, cisplatin-resistant 2780CP/Cl-16 ovarian tumor cells expressed a heterozygous, temperatur

114 he sensitization of folate receptor-alpha(+) ovarian tumor cells in vitro, this did not confer furthe

115 tatin either inside the peritoneum or by the ovarian tumor cells inhibited peritoneal seeding and dis

116 enetic inhibition of AXL in human metastatic ovarian tumor cells is sufficient to prevent the initiat

117 ckdown of endogenous testisin in NCI/ADR-Res ovarian tumor cells reduces PAR-2 N-terminal proteolytic

118 ts that do or do not express CTR1, and human ovarian tumor cells that are sensitive or resistant to c

119 ives epithelial-to-mesenchymal transition in ovarian tumor cells through beta-arrestin signaling.

120 dentified that DLX4 stimulates attachment of ovarian tumor cells to peritoneal mesothelial cells in v

121 esponse of primary patient-derived colon and ovarian tumor cells to therapy in mTiD cultures matched

122 onstrate that even though ABT-888 sensitizes ovarian tumor cells with functional HR to FdUrd, the eff

123 Finally, in vivo coinjection of ID8 mouse ovarian tumor cells with mouse embryonic fibroblasts sho

124 ression of the cell surface molecule CD44 in ovarian tumor cells, and inhibition of CD44 abrogated th

125 n was overexpressed in phosphaplatin-treated ovarian tumor cells, and platinum colocalized with FAS p

126 pe and destroyed autologous and immortalized ovarian tumor cells, following earlier pulsing with eith

127 onal regulation to target gene expression to ovarian tumor cells, holds promise as an effective thera

128 nt induced specific host immune responses to ovarian tumor cells, including the development of both C

129 ously been shown to inhibit proliferation of ovarian tumor cells, induce DNA damage and apoptosis in

130 ences of two genes that are highly active in ovarian tumor cells, MSLN and HE4, were used to target D

131 f cytokine production profiles revealed that ovarian tumor cells, tumor-derived fibroblasts, and anti

132 ll4 might induce Notch signaling in adjacent ovarian tumor cells.

133 large panel of both established and primary ovarian tumor cells.

134 anchorage-independent survival of breast and ovarian tumor cells.

135 d reports suggesting that it targets Pten in ovarian tumor cells.

136 o reduce E-cadherin levels in differentiated ovarian tumor cells.

137 eceptors and activate effector cells against ovarian tumor cells.

138 s of exome sequence data from 151 high-grade ovarian tumors characterized as part of the Cancer Genom

139 In ovarian tumors classified as indeterminate at ultrasonog

140 erium restores fertility to females carrying ovarian tumor (cystocyte overproliferation) mutant allel

141 n, primary, and metastatic serous epithelial ovarian tumors demonstrates that CDCP1 is expressed duri

142 c melanoma model and transplantable lung and ovarian tumors, demonstrating potential for broad clinic

143 ntly decreased cancer growth in mice bearing ovarian tumors derived from cisplatin-sensitive and -res

144 Ovarian tumor-derived cell lines MKP-Liver and MKP-Lung

145 Ovarian tumor-derived inflammatory factors stimulated ne

146 tinguishable disease, patients with advanced ovarian tumors display a broad range of survival end poi

147 The ovarian tumor domain (OTU) deubiquitinylating cysteine p

148 OTUD6B encodes a member of the ovarian tumor domain (OTU)-containing subfamily of deubi

149 Recent work has implicated the viral ovarian tumor domain (vOTU) as a possible nairovirus vir

150 Here, we demonstrate that the deubiquitinase ovarian tumor domain containing ubiquitin aldehyde bindi

151 Viral ovarian tumor domain proteases (vOTUs) are one of the tw

152 Deubiquitinating enzyme A (DUBA), an ovarian tumor domain-containing deubiquitinating enzyme,

153 PLP2 was also proposed to belong to the ovarian tumor domain-containing superfamily of deubiquit

154 Ovarian tumor domain-containing ubiquitin (Ub) aldehyde

155 of NF-kappaB, but the ubiquitin-editing OTU (ovarian tumor) domain is not.

156 Here we show that ovarian tumor endothelium displays high levels of HS seq

157 se to cps treatment of the immunosuppressive ovarian tumor environment, CD11c(+) cells regained the a

158 resistance in ovarian cancer cell lines and ovarian tumor explants.

159 more, CD44+/CD117+ cells isolated from human ovarian tumors express high levels of TG2.

160 iodiversity on deISGylating proteases of the ovarian tumor family (vOTU) from nairoviruses was evalua

161 arrying Brca1 mutations may be more prone to ovarian tumor formation after IR exposure than nonmutati

162 Transcriptomic analyses of the ovarian tumors from PGRB-overexpressing mice revealed en

163 PTUPB delayed the onset of debris-stimulated ovarian tumor growth and ascites leading to sustained su

164 e roles by which the HU177 epitope regulates ovarian tumor growth and provide new insight into the cl

165 GDKGE-containing collagen fragment inhibited ovarian tumor growth and the development of ascites flui

166 large tumor suppressor kinase-1 and regulate ovarian tumor growth by a yes-associated protein-depende

167 be an approach to suppress debris-stimulated ovarian tumor growth by preventing the therapy-induced s

168 Results Pazopanib inhibited ovarian tumor growth compared with control (0.054 g +/-

169 iferation, tube formation, angiogenesis, and ovarian tumor growth in mice.

170 this collagen epitope plays a role in SKOV-3 ovarian tumor growth in vivo.

171 arian cancer cells, but its contributions to ovarian tumor growth might be mediated through elements

172 In mice, high-fat diet (HFD) stimulation of ovarian tumor growth was remarkably suppressed by 1,25(O

173 rgeting ability and significantly suppressed ovarian tumor growth without causing toxicity to normal

174 stimulatory and contributed to inhibition of ovarian tumor growth.

175 ll infiltration, and experimental peritoneal ovarian tumor growth.

176 te protumorigenic factors that contribute to ovarian tumor growth.

177 peptide resulted in significant reduction in ovarian tumor growth.

178 Intraperitoneal ovarian tumors (Hey-A8 or OVCAR3) in mice enhanced on MR

179 Ovarian tumors homozygous for Trp53(R172H) mutation were

180 ncer cells and has beneficial effects on the ovarian tumor immune microenvironment.

181 genic mice vulnerable to carcinogenesis, and ovarian tumor implantation and development.

182 REG depletion retarded growth of xenografted ovarian tumors in mice, we generated a neutralizing mono

183 ater decrements in follicle numbers and more ovarian tumors in response to prenatal BaP exposure than

184 ICG) contrast agent can be used to visualize ovarian tumors in the peritoneal cavity by multimodal MR

185 luminescence images to measure the amount of ovarian tumors in the peritoneal cavity of mice.

186 hibition caused regression of ARID1A-mutated ovarian tumors in vivo.

187 onducted genomic analyses of intraperitoneal ovarian tumors in which adaptive resistance to anti-VEGF

188 Metastatic dissemination of ovarian tumors involves the invasion of tumor cell clust

189 Successful detection of orthotopic ovarian tumors is achieved by in vivo NIR-II imaging and

190 ferroptosis inducers significantly decrease ovarian tumor masses in mice.

191 We conclude that inflammation facilitates ovarian tumor metastasis by a mechanism largely mediated

192 varian tumors, TG2 promotes EMT and enhances ovarian tumor metastasis by activating oncogenic signali

193 In summary, TGF-beta-induced TG2 enhances ovarian tumor metastasis by inducing EMT and a cancer st

194 oneal inflammation plays a causative role in ovarian tumor metastasis, a poorly understood process.

195 ase in O-GlcNAcylation of tumor tissue in an ovarian tumor microarray.

196 together, our data suggest that MSCs in the ovarian tumor microenvironment have an expression profil

197 or instance, we established that MSCs in the ovarian tumor microenvironment promoted tumor growth and

198 Thus, chNKG2D T cells altered the ovarian tumor microenvironment to eliminate immunosuppre

199 Host components of the ovarian tumor microenvironment, notably peritoneal mesot

200 the first human MUC1-expressing, orthotopic ovarian tumor model, reveal novel MUC1 functions in ovar

201 ponse to treatment by bortezomib in a murine ovarian tumor model.

202 ies in both flank and orthotopic i.p. murine ovarian tumor models, as well as human tumor xenograft m

203 vivo MUC1-expressing conditional (Cre-loxP) ovarian tumor models, we focus here on MUC1 biology and

204 llowing in situ vaccination of an aggressive ovarian tumor mouse model (ID8-Defb29/Vegf-A).

205 interactions on ovarian follicle counts and ovarian tumor multiplicity at 7.5 months of age, with Gc

206 ation carriers are at risk for nonepithelial ovarian tumors, notably sex cord-stromal tumors.

207 We also find that the genes ovo and ovarian tumor (otu) are expressed in a female-specific m

208 Otubain 1 belongs to the ovarian tumor (OTU) domain class of cysteine protease de

209 positive-stranded RNA viruses that encode an ovarian tumor (OTU) domain DUB known as papain-like prot

210 es demonstrate that proteins that contain an ovarian tumor (OTU) domain possess deubiquitinating acti

211 interdependent activities of the A20 ZnF and ovarian tumor (OTU) domains that are inherent to the Ub

212 We recently identified that the ovarian tumor (OTU) family deubiquitinase OTULIN specifi

213 Sixteen ovarian tumor (OTU) family deubiquitinases (DUBs) exist

214 The ovarian tumor (OTU) family of deubiquitinases regulates

215 In contrast, we found that mutations in ovarian tumor (otu) interfere with both Sxl germline fun

216 The L protein has an ovarian tumor (OTU) protease domain located in the N ter

217 main at its N terminus, which belongs to the ovarian tumor (OTU) protease family.

218 The ovarian tumor (OTU) subfamily deubiquitinases have been

219 hly conserved deubiquitinating enzyme of the ovarian tumor (otubain) family, whose function has yet t

220 ovary, the majority of malignant epithelial ovarian tumors overexpressed IRS-1.

221 ociated with an increased risk of borderline ovarian tumors, particularly among women who had had mul

222 nd cell biological analysis of the resulting ovarian tumor phenotype.

223 KCiota frequent overexpression in high-grade ovarian tumors poses a novel pathway for therapeutic inv

224 ne tumors (SBOTs) are a challenging group of ovarian tumors positioned between benign and malignant d

225 etry-based proteomic characterization of 174 ovarian tumors previously analyzed by The Cancer Genome

226 eover, i.p. delivery of siKLF6-SV1 RNA halts ovarian tumor progression and improves median and overal

227 a useful new alternative strategy to control ovarian tumor progression based on selectively disruptin

228 e tumors, suggesting a role of IKKepsilon in ovarian tumor progression rather than in tumor initiatio

229 itoneal tumor-associated leukocytes inhibits ovarian tumor progression.

230 ts, suggesting an important role for RAD6 in ovarian tumor progression.

231 omentum tissue that promote endometrial and ovarian tumor proliferation, migration, and drug resista

232 In agreement with the ovarian tumor-promoting role of Neu5Ac, treatment with N

233 rts have identified a viral homologue of the ovarian tumor protease superfamily (vOTU) within its L p

234 oles in ovarian cancer cell survival and the ovarian tumor repressing effects of MLN4924 are unknown.

235 ography for direct functional measurement of ovarian tumor response to antiangiogenic therapy.

236 avity of mice bearing primary and metastatic ovarian tumors resulted in a significant reduction in tu

237 the authors identify that a subset of breast/ovarian tumors retain a normal allele, which is associat

238 xpression of PTB in a majority of epithelial ovarian tumors revealed by immunoblotting and tissue mic

239 surface epithelial cell line; and in 55% of ovarian tumor samples as compared with non-neoplastic ov

240 mework to measure the BRCAness of breast and ovarian tumor samples based on their gene expression pro

241 We then analyzed 91 ovarian tumor samples for mutations in TP53, BRAF, and K

242 ated MSCs (CA-MSCs) in the majority of human ovarian tumor samples that we analyzed.

243 ivity, YPEL3 gene expression is repressed in ovarian tumor samples.

244 The types of ovarian tumors should be given attention in future studi

245 ary breast tumors, and four sporadic primary ovarian tumors showed hypermethylation of the core promo

246 Infusing platelets into mice with orthotopic ovarian tumors significantly increased the proliferation

247 ome sequencing of nine non-serous epithelial ovarian tumors (six endometrioid and three mucinous) and

248 d that PTB was overexpressed in 17 out of 19 ovarian tumor specimens compared to their matched-normal

249 s a marker for microdissection, we find that ovarian tumor stromal cells harboring GT198 mutations ar

250 MMP-14 antibody disrupted ovarian tumor-stromal communication and was equivalent t

251 d intraperitoneally in mice are able to form ovarian tumors, suggesting that the EOC stem cells have

252 analysis of candidate genes at this locus in ovarian tumors supported a role for the BRCA1-interactin

253 by the microenvironment in RNASET2-mediated ovarian tumor suppression, which could eventually contri

254 cribe a novel interaction between the breast/ovarian tumor suppressor gene BRCA1 and the transcriptio

255 BRCA1 is a breast and ovarian tumor suppressor.

256 Highly expressed in ovarian tumors, TG2 promotes EMT and enhances ovarian tu

257 which, remarkably, are also misexpressed in ovarian tumors that arise from the loss of bag of marble

258 is a unifying protein driving metastasis in ovarian tumors that could be developed as an effective d

259 , we identified characteristics of breast or ovarian tumors that distinguished sporadic tumors from t

260 ed dynamic contrast-enhanced MRI to study 68 ovarian tumors that were classified as indeterminate at

261 sa of triple (MUC1KrasPten) Tg mice triggers ovarian tumors that, in analogy to human ovarian cancer,

262 lthough Maspin was expressed in some primary ovarian tumors, the promoter was epigenetically silenced

263 o test the efficacy of VLC elimination as an ovarian tumor therapy.

264 these data suggest that LPA initiates EMT in ovarian tumors through beta1-integrin-dependent activati

265 hat miR-204-5p could promote angiogenesis in ovarian tumors through THBS1.

266 12 studies participating in the Ovarian Tumor Tissue Analysis consortium contributed tis

267 as also elevated in metastatic and recurrent ovarian tumor tissue compared with patient-matched prima

268 Furthermore, immunohistochemical analysis of ovarian tumor tissue microarray detected aberrant ALK ex

269 tissue compared with patient-matched primary ovarian tumor tissue.

270 mic approach, we profiled 69 Chinese primary ovarian tumor tissues and found ALK to be aberrantly exp

271 analysis of PELP1/MNAR in normal and serous ovarian tumor tissues showed 3- to 4-fold higher PELP1/M

272 3(+) T-bet(+) Treg selectively accumulate in ovarian tumors to control type I T-cell responses, resul

273 ic therapy targeting HSulf-1 might sensitize ovarian tumors to conventional first-line therapies.

274 More importantly, this treatment sensitized ovarian tumors to low cisplatin concentrations.

275 emistry-based cytotoxic modality, sensitizes ovarian tumors to platinum agents and biologics and has

276 TAIR-EZH2 activity and resensitize resistant ovarian tumors to platinum.

277 The high frequency of relapse of epithelial ovarian tumors treated with standard chemotherapy has hi

278 et of 185 (90 optimal/95 suboptimal) primary ovarian tumors using the Affymetrix human U133A microarr

279 ere observed in recurrent platinum-resistant ovarian tumors vs primary ovarian tumors.

280 cer and 321 women with borderline epithelial ovarian tumors was carried out to test the association b

281 a preclinical mouse model for MUC1-positive ovarian tumors, we generated triple transgenic (Tg) mice

282 Xenograft studies with SKOV3 ovarian tumors were done using various C6.5/rGel constru

283 The ovarian tumors were positive for the epithelial marker c

284 cells isolated directly from CD133(-) human ovarian tumors were sufficient to generate tumors in imm

285 solid tumors, including breast, gastric, and ovarian tumors, where it offers a potential therapeutic

286 weeks of age, recapitulating human mucinous ovarian tumors, which also exhibit heterozygous TP53 mut

287 planation for the aggressive nature of human ovarian tumors with downregulated HtrA1.

288 ge III to IV extragonadal tumors or stage IV ovarian tumors with predicted LTDF survival < 70%.

289 Treatment of mice bearing established ovarian tumors with T cells expressing chimeric NKG2D re

290 Moreover, ovarian tumors with up-regulated PITX2 expression also s

291 P significantly reduced growth of orthotopic ovarian tumors, with CCPM-BIDEN-AP displaying greater an

292 umor tissues, such as germ cell, breast, and ovarian tumors, with in the latter case, evidence for a

293 he ovary constitute less than one percent of ovarian tumors worldwide.

294 tumor efficacy when dosed orally in an A2780 ovarian tumor xenograft model (TGI of 97% was observed o

295 In ovarian tumor xenograft models, Dll4 was expressed speci

296 tly suppressed the growth of intraperitoneal ovarian tumor xenografts outperforming their nontargeted

297 A greater amount of AON is delivered to ovarian tumor xenografts using the ternary copolymer-sta

298 eatment of mice harboring platinum-resistant ovarian tumor xenografts with pHLIP-PNA constructs suppr

299 pound caused regression of all treated A2780 ovarian tumor xenografts.

300 -3 cell lines and reduced tumor growth in an ovarian tumor xenographic model.