ライフサイエンスコーパス: ovarian tumor

1 obably by regulating alternative splicing of ovarian tumor.

2 ading domain mutations in three endometrioid ovarian tumors.

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

4 of peritoneal organs, particularly colon and ovarian tumors.

5 nomic relationship between these subtypes of ovarian tumors.

6 domain of DICER1 are common in nonepithelial ovarian tumors.

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

8 ay be an innovative therapeutic strategy for ovarian tumors.

9 RCA2 germline mutation-associated breast and ovarian tumors.

10 aining in peritoneal xenografts and in human ovarian tumors.

11 ermethylation in DNA derived from breast and ovarian tumors.

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

13 Two patients had ovarian tumors.

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

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

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

17 he development and maintenance of epithelial ovarian tumors.

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

19 n between IRS-1 expression and malignancy in ovarian tumors.

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

21 or-free survival in mice bearing established ovarian tumors.

22 ages to a phenotype similar to that found in ovarian tumors.

23 ressed the proliferation of ES-2 and OV-1063 ovarian tumors.

24 varian cancer in 106 stage III/IV epithelial ovarian tumors.

25 not in any of low-grade carcinomas or benign ovarian tumors.

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

27 platinum-resistant ovarian tumors vs primary ovarian tumors.

28 and its expression is markedly increased in ovarian tumors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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 he Brca1 wild-type and Brca1-deficient mouse ovarian tumors and cell lines provide a new experimental

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

46 lost or excluded from the nucleus in 85% of ovarian tumors and GATA4 expression is absent in majorit

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

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

49 ovarian carcinoma tissues relative to benign ovarian tumors and in ovarian carcinoma cell lines relat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 ecifically expressed within human and murine ovarian tumor ascites upon VLCs.

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

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

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

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

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

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

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

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

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

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

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

78 The chNKG2D T cells reduced the ovarian tumor burden using both cytotoxic and cytokine-d

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

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

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

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

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

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

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

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

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

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

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

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

91 ound that knockdown of PTB expression in the ovarian tumor cell line A2780 substantially impaired tum

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

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

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

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

96 3 leading to filamentous actin formation and ovarian tumor cell migration.

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

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

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

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

101 on and ErbB2/beta-catenin signaling in human ovarian tumor cells (SK-OV-3.ipl cells).

102 mice were able to reject a rechallenge with ovarian tumor cells 225 days after original tumor inject

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

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

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

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

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

108 The pellets of targeted ovarian tumor cells are treated by two different membran

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

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

111 We show that primary ovarian tumor cells express intracellular B7-H4, whereas

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

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

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

115 Implantation of human ovarian tumor cells into the ovaries of severe combined

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 Thus, the use of Hsp70-secreting ovarian tumor cells represents a potentially effective t

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

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

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

122 AS or BRAF mutations, we inactivated MAPK in ovarian tumor cells using CI-1040, a compound that selec

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

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

125 ls, but not ovarian epithelial or borderline ovarian tumor cells, although these benign cells indeed

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

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

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

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

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

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

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

133 B7-H4+ tumor macrophages, but not primary ovarian tumor cells, suppress tumor-associated antigen-s

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

135 y the consequences of EGFRvIII expression in ovarian tumor cells, we introduced EGFRvIII into the epi

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

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

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

139 eceptors and activate effector cells against ovarian tumor cells.

140 3zeta chain of the T-cell receptor to target ovarian tumor cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

156 Ovarian tumor domain-containing ubiquitin (Ub) aldehyde

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

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

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

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

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

162 Moreover, patients with ovarian tumors expressing higher levels of HSulf-1 showe

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

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

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

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

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

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

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

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

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

172 stimulatory and contributed to inhibition of ovarian tumor growth.

173 ll infiltration, and experimental peritoneal ovarian tumor growth.

174 te protumorigenic factors that contribute to ovarian tumor growth.

175 peptide resulted in significant reduction in ovarian tumor growth.

176 have previously shown that human epithelial ovarian tumors have increased levels of Cox-1, but not C

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

178 Ovarian tumors homozygous for Trp53(R172H) mutation were

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

180 ntitumor activities against established s.c. ovarian tumors in immunodeficient animals.

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

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

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

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

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

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

187 nges in KLF6 and KLF6-SV1 can directly alter ovarian tumor invasion and metastasis.

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

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

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

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

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

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

196 noma cells and interstitial collagens in the ovarian tumor microenvironment in inducing gene expressi

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

200 stimulates tumor metastasis in an orthotopic ovarian tumor model, which can be inhibited by a PI3K in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

226 itoneal tumor-associated leukocytes inhibits ovarian tumor progression.

227 e signaling pathways known to be critical in ovarian tumor progression.

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

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

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

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

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

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

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

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

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

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

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

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

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

241 ormed on 42 microdissected high-grade serous ovarian tumor samples.

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

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

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

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

246 An IgE Ab (MOv18 IgE) against an ovarian-tumor-specific Ag (folate binding protein), in c

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

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

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

250 We show that ovarian tumors strongly express CXC chemokine stromal-de

251 ved in a subset of primary breast, lung, and ovarian tumors suggesting potential utility in patient s

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

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

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

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

256 BRCA1 is a breast and ovarian tumor suppressor.

257 All primary ovarian tumors tested, regardless of their resistance to

258 Highly expressed in ovarian tumors, TG2 facilitates i.p. tumor dissemination

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

260 The molecular form of TA from ovarian tumor that activates cellular immunity is unknow

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

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

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

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

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

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

267 12 studies participating in the Ovarian Tumor Tissue Analysis consortium contributed tis

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

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

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

271 3(+) T-bet(+) Treg selectively accumulate in ovarian tumors to control type I T-cell responses, resul

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

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

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

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

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

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

278 for the first time the molecular profile of ovarian tumor vasculature.

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

280 1 as a potential molecular target of ATRA in ovarian tumors was assessed by immunohistochemistry in a

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

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

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

284 The ovarian tumors were positive for the epithelial marker c

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

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

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

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

289 imental findings, patient-derived epithelial ovarian tumors with low KLF6 and high KLF6-SV1 expressio

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

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

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

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

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

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

296 In ovarian tumor xenograft models, Dll4 was expressed speci

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

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

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

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