ライフサイエンスコーパス: ovarian

1 Negative and positive feedback effects of ovarian 17beta-estradiol (E2) regulating release of gona

2 nds because Ac workers have higher levels of ovarian activation than Am workers.

3 pies, including hepatocellular carcinoma and ovarian adenocarcinoma, Gadd45b inhibition in myeloid ce

4 Ovarian adenocarcinomas are shown to be an excellent mod

5 birth, as estimated by BOADICEA (Breast and Ovarian Analysis of Disease Incidence and Carrier Estima

6 diseases including various cancers (breast, ovarian and brain).

7 Treatment of HOTAIR-overexpressing ovarian and breast cancer cell lines with PNAs decreased

8 as an active, secreted peptide by epithelial ovarian and lung cancer cells in situ This finding promp

9 lnerabilities to overcome drug resistance in ovarian and other cancers.High-grade serous ovarian canc

10 , and perceived ability to evaluate uterine, ovarian, and musculoskeletal structures.

11 Our approach uncovers unique features of ovarian architecture and essential roles of vasculature

12 (MVI) has been found to be overexpressed in ovarian, breast and prostate cancers.

13 RNA expression from 67 ovarian CAF samples and 10 normal ovarian fibroblast (NO

14 0 scores, were associated with lower risk of ovarian cancer (comparing the highest quartile (4th) vs.

15 studies of Myc family targets in epithelial ovarian cancer (EOC) and neuroblastoma.

16 Epithelial ovarian cancer (EOC) has poor prognosis and rapid recurr

17 drug-repositioning candidates for epithelial ovarian cancer (EOC) have not been undertaken.

18 Epithelial ovarian cancer (EOC) is characterized by an immune suppr

19 Epithelial ovarian cancer (EOC) is the most fatal gynaecological ma

20 ociation between hysterectomy and epithelial ovarian cancer (EOC) was considered well established, in

21 e with prognosis in patients with epithelial ovarian cancer (EOC), but their prognostic importance an

22 therapy (NACT) for advanced-stage epithelial ovarian cancer (EOC).

23 High-grade serous ovarian cancer (HGSC) is an aggressive cancer with a wor

24 biomarkers for olaparib in high-grade serous ovarian cancer (HGSOC).

25 specially in patients with high-grade serous ovarian cancer (HGSOC).

26 l sonography (TVS) for women at high risk of ovarian cancer (OC) or fallopian tube cancer (FTC).

27 llion women have a history of breast (BC) or ovarian cancer (OC).

28 In high-grade serous ovarian cancer (OV), the bulk of genetic changes is not

29 Ovarian cancer (OvCa) cells are reported to undergo bioc

30 ation between PID and the risk of epithelial ovarian cancer according to tumor behavior and histotype

31 %, 1.0%) of 2763 patients were found to have ovarian cancer after an average follow-up of 5.1 years +

32 125 (CA-125), interpreted using the risk of ovarian cancer algorithm (ROCA), and transvaginal sonogr

33 38 years; IQR, 31-47 years) eligible for the ovarian cancer analysis, and 2213 women (median age, 47

34 51.4%) had a mother or sister with breast or ovarian cancer and 54 patients (48.6%) did not.

35 llected from patients with colon, breast, or ovarian cancer and cell lines harboring specific oncogen

36 studies have reported decreased incidence of ovarian cancer associated with regular intake of NSAIDs,

37 s, conducted between 1989 and 2009, from the Ovarian Cancer Association Consortium (OCAC), including

38 Patients with known ovarian cysts or ovarian cancer at time of the index CT examination were

39 was detected in 43 (68.3%) of 63 women with ovarian cancer but in none of 50 healthy controls.

40 The study was conducted among 415 ovarian cancer cases and 629 age- and site-matched contr

41 In vitro treatment of breast and ovarian cancer cell cultures in aqueous media by tamoxif

42 Suppressing KDM4B inhibits ovarian cancer cell invasion, migration and spheroid for

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

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

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

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

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

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

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

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

51 y against cisplatin-resistant A2780Cis human ovarian cancer cells (IC50 74 muM, blue light) with a ph

52 d platinum-sensitive and platinum- resistant ovarian cancer cells and ovarian cancer stem cells and (

53 l that EMT can be induced in epithelial-like ovarian cancer cells by co-expressing constitutively act

54 Silencing GPAM in ovarian cancer cells decreased cell migration and reduce

55 we showed that acquired cisplatin-resistant ovarian cancer cells expressed high levels of MKP-1 and

56 the tumor growth and migratory phenotypes of ovarian cancer cells expressing SHMT1 shRNAs.

57 aneously implanted cisplatin-resistant human ovarian cancer cells in athymic nude mice.

58 pithelial-to-mesenchymal transition (EMT) of ovarian cancer cells in vivo, STAT4 failed to induce EMT

59 parib) while overexpression of USP13 renders ovarian cancer cells resistant to chemotherapy.

60 ntiproliferative behavior against epithelial ovarian cancer cells resistant to cisplatin.

61 Thus, ovarian cancer cells seem to display heterogeneity in us

62 gulation of metastasis-associated behaviors, ovarian cancer cells that express low endogenous levels

63 s and reverses multi-drug resistance against ovarian cancer cells through downregulation of survivin.

64 Depleting or inhibiting USP13 sensitizes ovarian cancer cells to cisplatin and PARP inhibitor (ol

65 To evaluate whether the response of ovarian cancer cells to pitavastatin is potentiated by f

66 itaxel (PTX) and doxorubicin (DOX) resistant ovarian cancer cells to PTX and DOX by inhibiting surviv

67 Using pancreatic and ovarian cancer cells with ST6Gal-I knockdown or overexpr

68 its clonal growth, migration and invasion of ovarian cancer cells, whereas silencing in vivo inhibits

69 ociated neovasculature and on the surface of ovarian cancer cells.

70 d in vitro against both multiple myeloma and ovarian cancer cells.

71 n resulted in reduced SHMT1 transcription in ovarian cancer cells.

72 cid, risedronate and GGTI-2133 in a panel of ovarian cancer cells.

73 r with ERalpha/ERbeta-expressing SKOV3 human ovarian cancer cells.

74 plex is critical for sustained EMT traits of ovarian cancer cells.

75 ysis of 7 nested case-control studies in the Ovarian Cancer Cohort Consortium to investigate the asso

76 cancer screening studies, low prevalence of ovarian cancer consistently resulted in low positive pre

77 try-Medicare data, we assessed patients with ovarian cancer deceased in 2000 to 2012 with at least 13

78 I-MS as a powerful approach for rapid serous ovarian cancer diagnosis based on altered metabolic sign

79 acterization further supports the DNM3OS and ovarian cancer EMT connection.

80 on and their reproducible gene regulation in ovarian cancer EMT.

81 ngiogenesis) inhibitors such as pazopanib in ovarian cancer even when (18)F-FDG PET/CT does not indic

82 We demonstrate that ovarian cancer exhibits a targetable alteration in iron

83 rd of care for women with platinum-sensitive ovarian cancer following a complete or partial response

84 In addition, KDM3A induces ovarian cancer growth while antagonizing cellular senesc

85 nd potent antitumor efficacy in an ES-2-luc, ovarian cancer i.p. xenograft model.

86 metrial cancer in 53 of 196 (27%) women; and ovarian cancer in 15 (8%) of 196 women.

87 endometrial cancer in 83 (30%) of 279 women; ovarian cancer in 28 (10%) of 279 women; and colorectal

88 formed at the Center for Familial Breast and Ovarian Cancer in Cologne, Germany; data analysis, Novem

89 Epithelial ovarian cancer is a leading cause of death in gynecologi

90 Ovarian cancer is a lethal malignancy that has not seen

91 fibroblasts (CAFs) confer chemoresistance in ovarian cancer is poorly understood.

92 The current standard care of ovarian cancer is still cytoredutive surgery followed by

93 High-grade serous ovarian cancer is the most common ovarian cancer type.

94 Ovarian cancer is the most leading cause of cancer-relat

95 Ovarian cancer is usually diagnosed after metastasis.

96 function as a regulatory mechanism to impact ovarian cancer metastatic success.

97 ancers which can aid in the visualization of ovarian cancer micrometastasis.

98 ere we report an integrated analysis of >700 ovarian cancer molecular profiles, including genomic dat

99 ra-red fluorescence (NIRF) imaging on SKOV-3 ovarian cancer mouse model demonstrated that the NIR dye

100 use of targeted PARP-inhibitor therapies in ovarian cancer patients carrying deleterious missense RA

101 sh UBC as a promising therapeutic target for ovarian cancer patients with recurrent UBB silencing.

102 In matched samples from 11 high-grade serous ovarian cancer patients, we detected 2-20-fold more sN4

103 stress on chemosensitivity and prognosis of ovarian cancer patients.

104 ose abundance was increased in the plasma of ovarian cancer patients.

105 ases, and ascites cells isolated from serous ovarian cancer patients.

106 ons may present with a hereditary breast and ovarian cancer phenotype.

107 tanding the function of Nectin-4 shedding in ovarian cancer progression is critical to facilitate its

108 r pathways/transcription factors involved in ovarian cancer progression, poor clinical outcome, and c

109 proposed to be a pivotal cytokine promoting ovarian cancer progression.

110 an abnormal screening pelvic examination for ovarian cancer ranged from 5% to 36% at 1 year, with the

111 nknown adnexal cysts at CT was 6.6%, with an ovarian cancer rate of 0.7% (95% CI: 0.4%, 1.0%).

112 ublets are a standard of care for women with ovarian cancer recurring 6 months after completion of in

113 Ovarian cancer remains the most lethal gynecological mal

114 etween pelvic inflammatory disease (PID) and ovarian cancer risk are few and inconsistent.

115 n overall healthy dietary pattern may reduce ovarian cancer risk in African-American women, and parti

116 lthy Eating Index (AHEI)-2010-in relation to ovarian cancer risk in African-American women.

117 iation with PID, the association of PID with ovarian cancer risk is still somewhat uncertain and requ

118 een quartiles of dietary quality indices and ovarian cancer risk, adjusting for potential confounders

119 In the 4 ovarian cancer screening studies, low prevalence of ovar

120 s) and 80,672 Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (PLCO) ever-smoking parti

121 ut the PLCO (Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial) found no reduction.

122 formation of PGCCs and dedifferentiation in ovarian cancer specimens from patients treated with chem

123 platinum- resistant ovarian cancer cells and ovarian cancer stem cells and (ii) downregulation of bet

124 Only 40% of patients with advanced ovarian cancer survive more than 5 years.

125 sive boronate crosslinked micelles (BCM) for ovarian cancer therapy.

126 copy, can serve as indicators of response in ovarian cancer to multityrosine kinase inhibitor pazopan

127 NP(BTZ-DOX) exhibited significantly improved ovarian cancer treatment in SKOV-3 xenograft mouse model

128 may be an attractive therapeutic target for ovarian cancer treatment.

129 cision therapy opportunity for effective HGS ovarian cancer treatment.

130 otential clinical implications in breast and ovarian cancer treatment.

131 ve analysis of the metabolic requirements of ovarian cancer tumor growth has not been performed.

132 However, factors that drive HGS ovarian cancer tumor growth have not been fully elucidat

133 -omics profiles of primary high-grade serous ovarian cancer tumours (N=357) to delineate mechanisms u

134 ade serous ovarian cancer is the most common ovarian cancer type.

135 onment could enable peritoneal metastasis of ovarian cancer via induction of EMT program.

136 results showed that mRNA levels of IL-6R in ovarian cancer was positively associated with better pro

137 survival in patients with platinum-sensitive ovarian cancer who had achieved a response to platinum-b

138 Patients with suspected advanced-stage ovarian cancer who qualified for PCS were eligible.

139 In a luciferase-expressing ES-2 (ES-2-luc) ovarian cancer xenograft model, single i.p. injections o

140 hown that pitavastatin induces regression of ovarian cancer xenografts in mice.

141 We used the keywords "ovarian cancer" and searched through GEO database and fi

142 were diagnosed with breast cancer, 109 with ovarian cancer, and 245 with contralateral breast cancer

143 logical meaningful processes associated with ovarian cancer, such as CCL11, CCL16, CCL18, CCL23, CCL8

144 Poor prognosis of ovarian cancer, the deadliest of the gynecologic maligna

145 nal case of a patient with high-grade serous ovarian cancer, treated with multiple chemotherapy regim

146 subset of common types of cancer, including ovarian cancer, where NAPRT expression correlates with a

147 l opportunity to identify driver patterns in ovarian cancer, which will acquire some novel and clinic

148 neal xenografts and prolongs the survival of ovarian cancer-bearing mice.

149 in acquired resistance to platinum drugs in ovarian cancer.

150 trend = 0.01) were inversely associated with ovarian cancer.

151 LPP enhances the efficacy of chemotherapy in ovarian cancer.

152 eatic adenocarcinoma and advanced epithelial ovarian cancer.

153 reclinical models of advanced pancreatic and ovarian cancer.

154 serum biomarker and a therapeutic target for ovarian cancer.

155 sible role of tumoral expression of IL-6R in ovarian cancer.

156 as a novel therapeutic target for resistant ovarian cancer.

157 d may provide a new therapeutic strategy for ovarian cancer.

158 atinum-sensitive, relapsed high-grade serous ovarian cancer.

159 by mutated TP53, a gene commonly altered in ovarian cancer.

160 es in patients with suspected advanced-stage ovarian cancer.

161 M expression and reduced overall survival in ovarian cancer.

162 s (CAFs) contribute to the poor prognosis of ovarian cancer.

163 nvasive end-of-life care among patients with ovarian cancer.

164 intrabursal mouse xenograft models of human ovarian cancer.

165 logical function of IL-6R mRNA expression in ovarian cancer.

166 R) DNA repair genes are linked to breast and ovarian cancer.

167 inical trials in patients with leukaemia and ovarian cancer.

168 des a therapeutic strategy for highly lethal ovarian cancer.

169 urvival and chemoresistance in patients with ovarian cancer.

170 ted with 10 kilobase tandem duplications in ovarian cancer.

171 r use in liposomal form for the treatment of ovarian cancer.

172 nts with high grade but not low grade serous ovarian cancer.

173 n of CS-E, which is a possible biomarker for ovarian cancer.

174 n tissue phantoms and in an in vivo model of ovarian cancer.

175 le-appearing cysts were given a diagnosis of ovarian cancer.

176 mation and development of drug resistance in ovarian cancer.

177 tly is the best serum-based tumor marker for ovarian cancer.

178 a cell-line xenograft model of disseminated ovarian cancer.

179 and human myeloid dendritic cells (TIDC) in ovarian cancer.

180 nt and treatment of patients with breast and ovarian cancer.

181 target genes for future treatment efforts in ovarian cancer.

182 berrations responsible for poor prognosis in ovarian cancer.

183 n with endometrial cancer, and 49 women with ovarian cancer; mean follow-up was 68.2 months.

184 ovarian and other cancers.High-grade serous ovarian cancers (HGS-OvCa) frequently develop chemothera

185 fective chemotherapies for high-grade serous ovarian cancers (HGS-OvCa) has motivated a search for al

186 nificant prognostic value in both breast and ovarian cancers after considering established clinical v

187 tromal and tumour compartments of aggressive ovarian cancers and its levels correlate with poor clini

188 helicase is linked to hereditary breast and ovarian cancers as well as bone marrow failure disorder

189 ue microarray analysis revealed that >98% of ovarian cancers express the prolactin receptor (PRLR), f

190 Furthermore, UBR5 expression was higher in ovarian cancers from cisplatin-resistant patients than f

191 uppressive microenvironment, and response of ovarian cancers to immune therapies has thus far been di

192 ients with BRCA wild-type platinum-sensitive ovarian cancers who might benefit from rucaparib.

193 e-associated colorectal, endometrial, and/or ovarian cancers whose medical records were included in t

194 onsortium (OCAC), including 9,162 women with ovarian cancers, 2,354 women with borderline tumors, and

195 orse overall survival in breast, uterine and ovarian cancers.

196 ognosis and treatment response in breast and ovarian cancers.

197 olvement of this gene in the commencement of ovarian cancers.

198 ated in many colorectal, hepatocellular, and ovarian cancers.

199 gest a role for hormone-related exposures in ovarian carcinogenesis and risk factor differences by hi

200 Inflammation has been implicated in ovarian carcinogenesis.

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

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

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

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

205 relapsed peritoneal metastasis in epithelial ovarian carcinoma.

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

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

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

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

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

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

212 versely correlated with PKM2 levels in human ovarian carcinomas.

213 cells of periovulatory follicles and induces ovarian contraction.

214 lipid unsaturation is a metabolic marker for ovarian CSCs and a target for CSC-specific therapy.

215 al a novel mechanism by which KDM3A promotes ovarian CSCs, proliferation and chemoresistance and thus

216 and highlight the importance of considering ovarian cycle when studying the BLA of females.SIGNIFICA

217 5-102 years) had a newly detected finding of ovarian cyst described in the body or impression section

218 Patients with known ovarian cysts or ovarian cancer at time of the index CT

219 e to cope with two physiological challenges (ovarian development after queen loss and immune activati

220 The results revealed that OFM ovarian development can be divided into six stages.

221 During ovarian development, Rspo1 is a key factor required for

222 ns of ILP7 and ILP8 in lipid homeostasis and ovarian development.

223 ata are the first to investigate the role of ovarian E2 in young cycling females, and to identify a r

224 ere significantly impaired in the absence of ovarian Edn2 expression.

225 al, 11; prostate, 7; breast, 5; pancreas, 5; ovarian/endometrial/vulvar cancers, 3; and de novo chola

226 ot support the hypothesis that early loss of ovarian estrogens is a risk factor for type 2 diabetes.

227 Patients with platinum-resistant epithelial ovarian, fallopian tube, or primary peritoneal cancer re

228 While ovarian feedback on hypothalamo-pituitary function is a

229 on from 67 ovarian CAF samples and 10 normal ovarian fibroblast (NOF) samples were analysed to identi

230 stem cells in vitro, but generating a human ovarian follicle remains a challenge.

231 m cells can be induced to differentiate into ovarian follicle-like cells (FLCs) in vitro.

232 n (M105I mutation) causes early depletion of ovarian follicles and female subfertility.

233 w that a microfluidic system supports murine ovarian follicles to produce the human 28-day menstrual

234 rimordial germ cells, meiotic germ cells and ovarian follicles.

235 ween printed layers, affects the survival of ovarian follicles.

236 d serum estrogen and higher numbers of large ovarian follicles.

237 The balance between ovarian folliculogenesis and follicular atresia is criti

238 ourfold reduction in mTOR activity preserves ovarian function and normal birth numbers.

239 cal relevance of these observations to adult ovarian function is unknown.

240 to postmenopause, defined by a biomarker of ovarian function.

241 tin had, however, some protective effects on ovarian function.

242 tive Wnt signaling in subsets of pancreatic, ovarian, gastric, and colorectal tumors.

243 Transplantable murine models of ovarian high grade serous carcinoma (HGSC) remain an imp

244 POINTS: Despite an attenuated fluctuation in ovarian hormone concentrations in well-trained women, on

245 fect tied to elevated estrogen phases of the ovarian hormone cycle.

246 g-related outcomes may vary depending on the ovarian hormone levels.

247 Ovarian hormone signals regulate both the physiological

248 and interactive effects of intra-individual ovarian hormone variation and nicotine on suppression of

249 At the onset of puberty, ovarian hormones increase inhibitory tone in the prefron

250 y provide unique insight into the effects of ovarian hormones on the etiology and treatment of nicoti

251 These findings present an in vivo functional ovarian implant designed with 3D printing, and indicate

252 Premature ovarian insufficiency (POI) is a frequent long-term comp

253 One of the important causes of primary ovarian insufficiency is chemotherapy-induced primordial

254 y-four women (age 48 to 79 years) with focal ovarian lesions and 21 women (age 34 to 66 years) with f

255 = .0006), and nonvisualization of a discrete ovarian mass (P = .0037) were associated with shorter TT

256 In 8 patients (with either ovarian or endometrial cancer), after a staging lymphade

257 levels were upregulated in high-grade serous ovarian patient tumors, where the FoxM1 signature is amp

258 rovement in survival in a syngeneic model of ovarian peritoneal carcinomatosis.

259 heat-treated females that displayed a normal ovarian phenotype but with a "male-like" gonadal transcr

260 nctions executed by granulosa cells (GCs) in ovarian physiology, the role of multifunctional proteins

261 recurrent measurable or evaluable epithelial ovarian, primary peritoneal, or fallopian tube cancer, a

262 sensitive, high-grade serous or endometrioid ovarian, primary peritoneal, or fallopian tube carcinoma

263 part of the standard course of treatment for ovarian, prostate, colon, and bladder cancers.

264 noma skin cancer; breast; cervical; uterine; ovarian; prostate; testicular; kidney; bladder; brain an

265 mh and Sox9, and remarkable up-regulation of ovarian regulators, Cyp19a1 and Foxl2.

266 consequence of DICER1 deficit in colorectal, ovarian, renal and breast cancer cell lines.

267 rmine the associations between biomarkers of ovarian reserve and reproductive potential among women o

268 of evidence of their utility, biomarkers of ovarian reserve are being promoted as potential markers

269 uggest that anti-Mullerian hormone (AMH), an ovarian reserve marker, plays a physiological role outsi

270 herapy experience an accelerated loss of the ovarian reserve, leading to subfertility and infertility

271 cline in reproductive capacity, known as the ovarian reserve, until menopause.

272 atic retrotransposition events in high-grade ovarian serous carcinoma.

273 complex network of neuroendocrine and intra-ovarian signals.

274 cle, 9 patients had myomas, two patients had ovarian simple cysts, two endometrial cysts, three dermo

275 l carcinoma cell lines of gastric (MKN-45P), ovarian (SKOV-3), and colon (CT-26) origin, and that per

276 days after the injection of 2 x 10(6) human ovarian SKOV3 tumors cells into 14 female nude mice, tre

277 Therefore, we examined ovarian steroid hormone regulation of GPR64 expression i

278 on of ovarian steroids, yet they appear with ovarian steroid levels indistinguishable from those in w

279 be precipitated either by an acute change in ovarian steroid levels or by stable levels above a criti

280 ver-expression of ESC/E(Z) complex genes (an ovarian steroid-regulated gene silencing complex) in unt

281 s in the cognitive and behavioral effects of ovarian steroids in women, and may provide a neurogeneti

282 pression and stimulated by administration of ovarian steroids, yet they appear with ovarian steroid l

283 mong women, reflect abnormal responsivity to ovarian steroids.

284 c disorder (PMDD) symptoms are eliminated by ovarian suppression and stimulated by administration of

285 memory task during three hormone conditions: ovarian suppression induced by the gonadotropin-releasin

286 Ovarian teratoma was most common and was predicted best

287 metabolic profiles of HGSC, BOT, and normal ovarian tissue samples.

288 zation that has been noted in the context of ovarian tissue transplantation.

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

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

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

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

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

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

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

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

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

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

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

300 ading domain mutations in three endometrioid ovarian tumors.