ライフサイエンスコーパス: ovarian cancer

1 bine in platinum-resistant high-grade serous ovarian cancer.

2 imens from 20 human patients with epithelial ovarian cancer.

3 ty of people with colorectal, endometrial or ovarian cancer.

4 kly treatment among patients with epithelial ovarian cancer.

5 me stability underlies hereditary breast and ovarian cancer.

6 ncer phenotype, is the most common malignant ovarian cancer.

7 kinase AXL to induce oncogenic signaling in ovarian cancer.

8 -200 (miR-200) family is highly expressed in ovarian cancer.

9 rian cancer, 20.4% were diagnosed with a non-ovarian cancer.

10 alpha to regulate an inflammatory network in ovarian cancer.

11 facilitating tumorigenesis and metastasis of ovarian cancer.

12 oinciding with poor outcome in patients with ovarian cancer.

13 vel EphB4-based therapeutic approach against ovarian cancer.

14 tment option for platinum-eligible recurrent ovarian cancer.

15 h newly diagnosed, advanced-stage epithelial ovarian cancer.

16 -emitting radionuclides for the treatment of ovarian cancer.

17 72-positive xenografts in a murine model of ovarian cancer.

18 tly associated with lower odds of epithelial ovarian cancer.

19 therapeutic target for paclitaxel-resistant ovarian cancer.

20 high concentrations in ascites of women with ovarian cancer.

21 cing in flank and metastatic mouse models of ovarian cancer.

22 cy to gemcitabine alone in high-grade serous ovarian cancer.

23 e of powder in the genital area and incident ovarian cancer.

24 ritic cell vaccines and immunosuppression in ovarian cancer.

25 ic cytokines and chemokines overexpressed in ovarian cancer.

26 ith ovarian cancer and 1,321 (2.6%) with non-ovarian cancer.

27 genesis and altered immunogenic responses in ovarian cancer.

28 pe (SCCOHT) is a rare and aggressive form of ovarian cancer.

29 les in BRIP1 confer risk for both breast and ovarian cancer.

30 apeutic intervention of metastatic spread in ovarian cancer.

31 95% CI, 0.91-1.05]; P = .55) with epithelial ovarian cancer.

32 py, with potential application to metastatic ovarian cancer.

33 sk, ranges from 12 for testicular to 2.5 for ovarian cancer.

34 f the AXL signaling axis in PIK3R2-amplified ovarian cancer.

35 xt-specific, pro-metastatic role of SIRT3 in ovarian cancer.

36 compared with breast, prostate, uterine, and ovarian cancer.

37 aged <50 years and 15.2% aged >=50 years had ovarian cancer.

38 the genital area and self-reported incident ovarian cancer.

39 ostic significance in patients with advanced ovarian cancer.

40 ood biomarkers for both human and laying hen ovarian cancer.

41 opens the door to targeted immunotherapy for ovarian cancer.

42 egimens in the management of newly diagnosed ovarian cancer.

43 novel therapies for this aggressive form of ovarian cancer.

44 biopsies from patients with glioblastoma and ovarian cancer.

45 buting to the poor prognosis associated with ovarian cancer.

46 ating regions, superenhancers, and breast or ovarian cancers.

47 ety in a range of neoplasms, particularly in ovarian cancers.

48 ry care for the detection of ovarian and non-ovarian cancers.

49 ved for the treatment of advanced breast and ovarian cancers.

50 CD49e+ CAF compartment in high-grade serous ovarian cancers.

51 primarily associate with familial breast and ovarian cancers.

52 ncing antitumor efficacy in breast, lung and ovarian cancers.

53 ong whom 3,246 developed invasive epithelial ovarian cancer (2,045 serous, 319 endometrioid, 184 muci

54 le breast cancer, 5% (95% CI, 2% to 10%) for ovarian cancer, 2%-3% (95% CI females, 1% to 4%; 95% CI

55 ho were aged >=50 years and who did not have ovarian cancer, 20.4% were diagnosed with a non-ovarian

56 steroid hormone pathway activation, whereas ovarian cancer 3D cultures with miR-200 knockdown showed

57 person-years at risk), 2168 women developed ovarian cancer (58 cases/100 000 person-years).

58 leads to small increases in the risk of most ovarian cancers, a risk that cumulates through life, sug

59 A patient with advanced germline BRCA1 ovarian cancer achieved RECISTv1.1 partial response and

60 retrospective cohort analyses of epithelial ovarian cancer among BRCA1/2 mutation carriers in the Co

61 A125 testing; 456 (0.9%) were diagnosed with ovarian cancer and 1,321 (2.6%) with non-ovarian cancer.

62 A sample included 3887 women with epithelial ovarian cancer and 27 561 control individuals.

63 cluded 22 406 women with invasive epithelial ovarian cancer and 40 941 control individuals and the CI

64 ts to determine the estimated probability of ovarian cancer and all cancers at any CA125 level and ag

65 ion of Gynecology and Obstetrics stage IC-IV ovarian cancer and an Eastern Cooperative Oncology Group

66 relative to the internal control miR-103a in ovarian cancer and control blood specimens collected fro

67 isms of genome stability that lead to CIN in ovarian cancer and demonstrate the benefit of integratin

68 BRD9 is overexpressed in ovarian cancer and depleting BRD9 sensitizes cancer cell

69 a maintenance therapy in platinum-sensitive ovarian cancer and gastric cancer.

70 one modifications are being characterized in ovarian cancer and have been functionally linked to proc

71 of BRIP1 may confer risk for both breast and ovarian cancer and highlight the importance of functiona

72 t the RNA abundance of EIF3C is increased in ovarian cancer and positively correlates with the protei

73 d from H3K27Ac ChIP-seq data generated in 26 ovarian cancer and precursor-related cell and tissue typ

74 pseudouridine may be a novel risk factor for ovarian cancer and that TAGs may also be important, part

75 represents a potential novel risk factor for ovarian cancer and triglycerides may be important partic

76 YTHDF1 is frequently amplified in ovarian cancer and up-regulation of YTHDF1 is associated

77 residual familial aggregation of breast and ovarian cancer and were adjusted for the family-specific

78 ncers, including glioma, endometrial cancer, ovarian cancer, and breast cancer.

79 hypercholesterolemia, hereditary breast and ovarian cancer, and Lynch syndrome.

80 ad is the primary mechanism of metastasis of ovarian cancer, and survival of ovarian cancer cells in

81 , when monoallelic, predispose to breast and ovarian cancer, and when biallelic, result in a severe s

82 Advanced ovarian cancers are a leading cause of cancer-related de

83 of invasive epithelial ovarian cancer in the Ovarian Cancer Association Consortium (OCAC; N = 63 347)

84 otypic chemosensitivity assay for epithelial ovarian cancer based on Doppler spectroscopy of infrared

85 There are three types of ovarian cancer based on histopathological examination: b

86 Additionally, ovarian cancer-bearing mice treated with ITLN1 demonstra

87 The ovarian cancer biomarker HE4 is known to promote prolife

88 n cancer (general population) and epithelial ovarian cancer (BRCA1/2 mutation carriers), measured as

89 how a unique collagen fragment may regulate ovarian cancer, but in addition may help provide a usefu

90 nhibition has yielded encouraging results in ovarian cancer, but predictive biomarkers are lacking.

91 n extremely high lifetime risk of breast and ovarian cancer, but the exact mechanism by which the BRC

92 d expression transiently increased following ovarian cancer cell detachment and in tumor cells derive

93 in vitro inhibitor of PTP4A3 and human A2780 ovarian cancer cell growth was reduced.

94 TLN1 suppresses lactotransferrin's effect on ovarian cancer cell invasion potential and proliferation

95 studies performed in uMUC1-expressing human ovarian cancer cell line SKOV3/Luc and control uMUC1(low

96 er agents, we developed and characterized an ovarian cancer cell line that is resistant to a previous

97 This TRIP-resistant ovarian cancer cell line, A2780TR, was found to be 9 tim

98 tive to TRIP compared to the wild-type A2780 ovarian cancer cell line.

99 In this study, we cultured ovarian cancer cell lines in adherent and nonadherent co

100 s9-mediated deletion of DAB2IP in epithelial ovarian cancer cell lines upregulated expression of stem

101 igen presentation complex in human and mouse ovarian cancer cell lines.

102 AR-3, SKOV-3, and TYKNu) and one mouse (ID8) ovarian cancer cell lines.

103 monstrate that antiproliferative activity in ovarian cancer cells (OVCAR8) depends on CDK2 degradatio

104 ivo models we show that secondary epithelial ovarian cancer cells (sEOC) do not fully reacquire the m

105 lysosomal beta-gal detection and imaging in ovarian cancer cells (SKOV-3 cells).

106 silenced, HR+, CARM1-high, high-grade serous ovarian cancer cells become PARPi sensitive, undergo mit

107 tential of Lyso-Gal for detection of primary ovarian cancer cells by using beta-gal as the biomarker.

108 , these results show that targeting FABP4 in ovarian cancer cells can inhibit their ability to adapt

109 the critical regulator of lipid responses in ovarian cancer cells cocultured with adipocytes.

110 tes binding to its cognate receptor CCR-2 on ovarian cancer cells facilitates migration and omental m

111 ibitor TMI-1 or by shRNA knockdown prevented ovarian cancer cells from releasing TNF-alpha protein in

112 olecular signature of the primary epithelial ovarian cancer cells from which they are derived.

113 Highly selective imaging of ovarian cancer cells has been achieved upon incubation w

114 etastasis of ovarian cancer, and survival of ovarian cancer cells in the peritoneal cavity as nonadhe

115 TGFbeta reduces MHC-I expression in ovarian cancer cells in vitro.

116 Uncontrolled growth of ovarian cancer cells is the fifth leading cause of femal

117 tor) reduced growth and peritoneal spread of ovarian cancer cells more effectively than either single

118 Here we report that ovarian cancer cells overexpressing glutaminase (GLS), a

119 iated knockout of FABP4 in high-grade serous ovarian cancer cells reduced metastatic tumor burden in

120 nisms that govern this metastatic process in ovarian cancer cells remain poorly understood.

121 s study describes the mechanism exhibited by ovarian cancer cells required for adherent cell transiti

122 chymal transition is required for epithelial ovarian cancer cells to acquire metastatic potential, th

123 Adipocytes are critical for ovarian cancer cells to home to the omentum, but the met

124 d differences in the resistance responses of ovarian cancer cells to TRIP and conventional drugs.

125 Therapeutically, p85beta expression renders ovarian cancer cells vulnerable to inhibitors of AXL, p1

126 FZD7(+) platinum-tolerant ovarian cancer cells were more sensitive and underwent f

127 target genes IL8 and HIF1A in immune cells, ovarian cancer cells, and endothelial cells.

128 f the MYC oncogene in tumor cells, including ovarian cancer cells, correlates with poor responses to

129 we systematically assessed in vivo growth of ovarian cancer cells, including six validated HGSC cell

130 ignaling and suppressed stemness features of ovarian cancer cells.

131 ne sets regulated by miR-200 in both OSE and ovarian cancer cells.

132 GLS-expressing but not in low GLS-expressing ovarian cancer cells.

133 e a vital biomarker overexpressed in primary ovarian cancer cells.

134 inflammatory mediators in response to LPA in ovarian cancer cells.

135 n for visualization and diagnosis of primary ovarian cancer cells.

136 le for the transactivation of EGFR by LPA in ovarian cancer cells.

137 to disrupt peritoneal spread and adhesion of ovarian cancer cells.

138 ion and epithelial-mesenchymal transition of ovarian cancer cells.

139 pha mRNA and release of TNF-alpha protein in ovarian cancer cells.

140 activates the IGF1R/STAT3 signaling axis in ovarian cancer cells.

141 and inducing a metabolic shift in metastatic ovarian cancer cells.

142 CA125 is a useful test for ovarian cancer detection in primary care, particularly i

143 urrent, platinum-resistant high-grade serous ovarian cancer (determined histologically) and Eastern C

144 tical inclusion cyst involvement in sporadic ovarian cancer development.

145 Ovarian and non-ovarian cancers diagnosed in the year following CA125 te

146 lthough ovarian cancer is rare, risk of most ovarian cancers doubles as the number of lifetime ovulat

147 The motility of SKOV-3 epithelial ovarian cancer (EOC) cells has been shown to be dependen

148 Epithelial ovarian cancer (EOC) is a highly lethal gynecologic mali

149 Epithelial ovarian cancer (EOC) is a leading cause of cancer-relate

150 Epithelial ovarian cancer (EOC) is the most lethal of gynecologic m

151 Epithelial ovarian cancer (EOC) metastasis occurs by exfoliation of

152 cles that play important roles in epithelial ovarian cancer (EOC) progression, as they are constantly

153 D2L2 and sensitizes HR-proficient epithelial ovarian cancer (EOC) to poly(adenosine diphosphate-ribos

154 9 regions associated with risk of epithelial ovarian cancer (EOC).

155 kade exhibits limited efficacy in epithelial ovarian cancer (EOC).

156 r and PARP inhibitor to treat chemoresistant ovarian cancers, especially those with high GLS expressi

157 majority of women diagnosed with epithelial ovarian cancer eventually develop recurrence, which rapi

158 s fluid and tissue slices from patients with ovarian cancer facilitated characterization of patients

159 In a mouse model of metastatic ovarian cancer, fluorescently labeled silica, poly(lacti

160 In high-grade serous ovarian cancer, Galgo signatures obtained similar predic

161 l and histotype-specific invasive epithelial ovarian cancer (general population) and epithelial ovari

162 and histone modifications as "clothes of the ovarian cancer genome" in relationship to their function

163 women with high CA125 levels, especially if ovarian cancer has been excluded, in order to prevent di

164 Ovarian cancer has few known risk factors, hampering ide

165 Ovarian cancer has thus far been refractory to immunothe

166 cer syndromes, such as hereditary breast and ovarian cancer (HBOC), consider genetic testing, especia

167 onditions-BRCA-related hereditary breast and ovarian cancer (HBOC), Lynch syndrome (LS) and familial

168 ops in women with advanced high-grade serous ovarian cancer (HGSOC) and is associated with drug resis

169 High grade serous ovarian cancer (HGSOC) is a fatal gynecologic malignancy

170 ant chemotherapy (NACT) in high-grade serous ovarian cancer (HGSOC), we performed immunogenomic analy

171 the clinical management of high grade serous ovarian cancer (HGSOC).

172 (g)(2)) of EOC overall and high-grade serous ovarian cancer (HGSOCs) were estimated to be 5%-6%.

173 gh-grade serous, endometrioid, or clear cell ovarian cancer in clinical complete response after a com

174 widely used as an investigation for possible ovarian cancer in symptomatic women presenting to primar

175 case-control analyses of invasive epithelial ovarian cancer in the Ovarian Cancer Association Consort

176 nts associated with hereditary breast and/or ovarian cancer in two children, a likely pathogenic vari

177 Clinicians should also consider non-ovarian cancers in women with high CA125 levels, especia

178 Ovarian cancer incidence was 61 cases/100 000 person-yea

179 etabolites (N = 420) with risk of epithelial ovarian cancer, including both borderline and invasive t

180 ults aged 15 to 25 years with non-epithelial ovarian cancers, including malignant ovarian germ cell t

181 ween the evanescent fields of microfiber and ovarian cancer inter-cellular medium at different treatm

182 ls and adipocytes, as a primary regulator of ovarian cancer intraperitoneal metastatic dissemination

183 Ovarian cancer is a deadly disease that afflicts ~22,000

184 Ovarian cancer is an aggressive epithelial tumor that re

185 etween use of powder in the genital area and ovarian cancer is not established.

186 Although ovarian cancer is rare, risk of most ovarian cancers dou

187 Although the 10-year absolute risk of ovarian cancer is small, it roughly doubles as the numbe

188 A major clinical challenge of ovarian cancer is the development of malignant ascites a

189 Ovarian cancer is the fifth cause of cancer-related mort

190 Because ovarian cancer is the fifth most common cause of cancer

191 carcinoma (HGSC), the most common subtype of ovarian cancer, is the major cause of death due to gynec

192 efficacy of gemogenovatucel-T in front-line ovarian cancer maintenance.

193 ovel congeners in triple negative breast and ovarian cancers, malignancies that typically succumb to

194 tivity occurs in multiple cancers, including ovarian cancer, medulloblastoma, breast cancer, colorect

195 unreported role for host-expressed Wnt5a in ovarian cancer metastasis and suggest Fgr as a novel tar

196 egulation of gene signatures associated with ovarian cancer metastasis, and reduced clonogenic cancer

197 han in normal omentum, the preferred site of ovarian cancer metastasis.

198 is study, we elucidated the role of Wnt5a in ovarian cancer metastasis.

199 ntestinal function in a preclinical model of ovarian cancer metastasis.

200 ortunity for specific metabolic targeting of ovarian cancer metastasis.

201 Ovarian cancer metastatic progression can be restricted

202 gest Fgr as a novel target for inhibition of ovarian cancer metastatic progression.Significance: This

203 st cancer; germline BRCA-mutated, metastatic ovarian cancer; metastatic gastric cancer; and relapsed

204 of this approach was further validated in an ovarian cancer model with typical germline mutations (ID

205 ns, as well as from a laying hen spontaneous ovarian cancer model.

206 s were identified using in vitro and in vivo ovarian cancer models treated repetitively with carbopla

207 Here, we describe a "living biobank" of ovarian cancer models with extensive replicative capacit

208 PXN silencing in ovarian cancer mouse models reduced angiogenesis, tumor

209 I/II trial of niraparib and pembrolizumab in ovarian cancer (NCT02657889).

210 sequences of somatic non-coding mutations in ovarian cancer (OC) are unknown.

211 nment (TME) and ascites-derived spheroids in ovarian cancer (OC) facilitate tumor growth and progress

212 Ovarian cancer (OC) incidence and mortality rates differ

213 ast cancer (BC), pancreatic cancer (PC), and ovarian cancer (OC) susceptibility.

214 In ovarian cancer (OC), IL-17-producing T cells (Th17s) pre

215 fficacy in triple negative breast (TNBC) and ovarian cancers (OCs) harboring BRCA mutations, generati

216 cer (BRCA1/2 mutation carriers), measured as ovarian cancer odds (general population) and hazard rati

217 was associated with lower odds of epithelial ovarian cancer (odds ratio [OR], 0.60 [95% CI, 0.43-0.83

218 cohorts of patients with advanced, recurrent ovarian cancer or malignant mesothelioma received anetum

219 ed with a 2.5-fold increased risk of overall ovarian cancer (OR = 2.56; 95% CI, 1.48-4.45; P = 0.001/

220 g ever users, compared with never users, for ovarian cancer [OR = 0.72; 95% confidence interval (CI),

221 d that targeting peritoneal LPMs may improve ovarian cancer outcomes.

222 The majority of women with recurrent ovarian cancer (OvCa) develop malignant ascites with vol

223 Ovarian cancer (OVCA) inevitably acquires resistance to

224 plicated in the progression and prognosis of ovarian cancer (OvCa).

225 ue of 53 U/ml equated to a 3% probability of ovarian cancer overall.

226 HE4 and IL8 levels positively correlated in ovarian cancer patient tissue.

227 High-grade serous ovarian cancer patient tumors and cells express signific

228 ing cause of female cancer deaths since most ovarian cancer patients are diagnosed at an advanced sta

229 eaming' germline BRCA testing pathway in 255 ovarian cancer patients at Imperial College NHS Trust.

230 A germline BRCA mutation (BRCAm) in ovarian cancer patients provides prognostic and predicti

231 expressed in high-grade serous carcinoma of ovarian cancer patients, and its expression is even high

232 of ~6,000 FTE cells, predominantly from non-ovarian cancer patients, identified 6 FTE subtypes.

233 LPA), a lipid mediator present in ascites of ovarian cancer patients, induced expression of TNF-alpha

234 tes with the protein expression of YTHDF1 in ovarian cancer patients, suggesting modification of EIF3

235 arget of MCP-1/CCR-2 axis that could benefit ovarian cancer patients.

236 is associated with the adverse prognosis of ovarian cancer patients.

237 ade serous carcinoma (HGSC), the most common ovarian cancer, posits to its development in fallopian t

238 the curve (AUC) value of 0.904 for American ovarian cancer prediction, whereas a model consisting of

239 lly actionable gene implicated in breast and ovarian cancer predisposition that has become a high pri

240 n can be an effective therapeutic target for ovarian cancer prevention or treatment.

241 cin 1 (uMUC1) tumor antigen, a biomarker for ovarian cancer progression and response to therapy, usin

242 ify the novel YTHDF1-EIF3C axis critical for ovarian cancer progression which can serve as a target t

243 e omental tumor microenvironment facilitates ovarian cancer progression.

244 ore presents a promising strategy to prevent ovarian cancer recurrence and has potential for clinical

245 ate ovarian cancer stem cells and to prevent ovarian cancer recurrence.

246 Ovarian cancer remains a significant challenge in women

247 ding to the abnormal TNF-alpha expression in ovarian cancer remains poorly understood.

248 emerging paradigm is changing many facets of ovarian cancer research and routine gynecology practice.

249 -onset breast cancer and 1,199 patients with ovarian cancer revealed nearly 2% of patients carry a ve

250 ductase inhibition was associated with lower ovarian cancer risk (hazard ratio, 0.69 [95% CI, 0.51-0.

251 n ever use of powder in the genital area and ovarian cancer risk among women with a patent reproducti

252 relationship between incessant ovulation and ovarian cancer risk in order to identify mechanisms of c

253 vulatory cycles (LOC) and its components and ovarian cancer risk overall and by histotype.

254 hemopreventive role of statins in epithelial ovarian cancer risk.

255 er a woman's reproductive years may increase ovarian cancer risk.

256 8; 95% CI, 5.82 to 8.85; P = 6.5 x 10(-76)), ovarian cancer (RR, 2.91; 95% CI, 1.40 to 6.04; P = 4.1

257 eld-out testing dataset of 108 breast and 62 ovarian cancer samples, our method ranked first in both

258 rol study within the United Kingdom Trial of Ovarian Cancer Screening (UKCTOCS).

259 in the PLCO (Prostate, Lung, Colorectal, and Ovarian) Cancer Screening Trial (n = 41 856).

260 Ovarian cancer selective metastasizes to the omentum con

261 d with clear cell, endometrioid, or mucinous ovarian cancer should be offered somatic tumor testing f

262 All women diagnosed with epithelial ovarian cancer should have germline genetic testing for

263 Women with epithelial ovarian cancer should have testing at the time of diagno

264 s to neoadjuvant chemotherapy for epithelial ovarian cancer should not be used as individual predicti

265 High-grade serous ovarian cancers show increased replication stress, rende

266 ysis showed that overexpression of DAB2IP in ovarian cancer significantly altered stemness-associated

267 Here we show that NGH in serous ovarian cancer (SOC) can be accurately measured when inf

268 Atlas (TCGA) database and in residual human ovarian cancer specimens after chemotherapy.

269 spersed-settled cells obtained from cultured ovarian cancer spheroids.

270 Persistence of ovarian cancer stem cells (OCSC) at the end of therapy m

271 way inhibitor has the potential to eradicate ovarian cancer stem cells and to prevent ovarian cancer

272 though the MEK Inhibitor in Low-Grade Serous Ovarian Cancer Study did not meet its primary end point,

273 State-of-the art therapy for recurrent ovarian cancer suitable for platinum-based re-treatment

274 rmline genetic testing for BRCA1/2 and other ovarian cancer susceptibility genes.

275 uce Famdenovo.BRCA for hereditary breast and ovarian cancer syndrome and apply it to a small set of f

276 almost twice as likely to be diagnosed with ovarian cancer than women in the 10th percentile (<294)

277 In a mouse model of non-resectable ovarian cancer, the cell-loaded nitinol thin films spati

278 Novel therapies are urgently needed for ovarian cancer, the deadliest gynecologic malignancy.

279 g for all women with non-mucinous epithelial ovarian cancer, there is significant variability in acce

280 l carcinoma (OCCC), a challenging subtype of ovarian cancer, this problem is compounded by near-unive

281 ignancies, such as cervical, endometrial and ovarian cancers, through direct and indirect mechanisms,

282 of N-glycans from human laryngeal cancer and ovarian cancer tissues.

283 limited efficacy of tocilizumab observed in ovarian cancer to date.

284 In metastatic ovarian cancer, total abdominal irradiation (TAI) was us

285 Yet the antioxidant adaptations required for ovarian cancer transcoelomic metastasis, which is the pa

286 itaxel resistance is a critical challenge in ovarian cancer treatment.

287 sm gene sets were strongly correlated in the ovarian cancer Tumor Cancer Genome Atlas (TCGA) database

288 Deaths from ovarian cancer usually occur when patients succumb to ov

289 Advanced ovarian cancer usually spreads to the omentum.

290 Here, using multi-omics analysis for ovarian cancer, we identified a novel mechanism involvin

291 ioritize potential points of intervention in ovarian cancer, we identified the lysine rich coiled-coi

292 ulatory elements influence predisposition to ovarian cancer, we used motifbreakR to predict the disru

293 The effects of miR-522-3p and E2F2 in ovarian cancer were examined using public databases, rev

294 st cancer, two with lung cancer and one with ovarian cancer-were enrolled into the pre-specified eval

295 cohort of >117,000 patients with breast and ovarian cancer who underwent panel testing, the combined

296 ond-degree blood relatives of a patient with ovarian cancer with a known germline pathogenic cancer s

297 Treating mice bearing ID8 Trp53-/- ovarian cancer with HDAC6i/DNMTi led to an increase in t

298 y exerting synergistic anti-tumor effects on ovarian cancers with PTEN deficiency and KRAS(G12D) muta

299 2 mAb, also mediated improved survival in an ovarian cancer xenograft model.

300 A panel of patient-derived ovarian cancer xenografts (PDX), similar in genetics and