ライフサイエンスコーパス: HGSOC

1 HGSOC spreads when single cells and spheroids detach, fl

2 HGSOC tumors exhibit genomic instability with frequent a

3 an interval to diagnosis of 9 (TNBC) and 10 (HGSOC) years.

4 is associated with shorter survival in 1000 HGSOC patients.

5 tion, we used bulk RNA-seq data covering 342 HGSOC patients from The Cancer Genome Atlas (TCGA) and d

6 exhibits in vivo single agent efficacy in a HGSOC-PDX with reduced sensitivity to PARPi by overcomin

7 need to understand antitumor immunity across HGSOC sites.

8 vironment in STICs that persists in advanced HGSOC.

9 he tumor-immune microenvironment of advanced HGSOC is intrinsically heterogeneous and that chemothera

10 ral anticancer activities, including against HGSOC, but has limited use in vivo.

11 alterations (SCNAs) in frequently amplified HGSOC cancer genes significantly correlate with gene exp

12 ival pathway in the context of MYC-amplified HGSOC is statistically associated with increased prevale

13 s molecular subtyping of prostate cancer and HGSOC with commonly used sample annotation tools in a si

14 ed to address the challenges of prostate and HGSOC molecular classification.

15 informatics training to explore prostate and HGSOC transcriptional data without the need for extensiv

16 oncogenic p53 mutations in LPA signaling and HGSOC progression through regulation of ACP6 expression.

17 s with time-to-disease progression (TTP) and HGSOC transcriptomic profiles (Classification of Ovarian

18 Both HGSOC cell lines are cisplatin resistant, and we used er

19 ors from patients with PARPi-resistant BRCAm HGSOC, and high coexpression of DHX9 and AKT1 correlated

20 th PARPi-sensitive and PARPi-resistant BRCAm HGSOC.

21 roach to overcome CHK1i resistance in BRCAwt HGSOC.

22 We report that BRCAwt HGSOC develops resistance to prexasertib monotherapy via

23 ertib monotherapy in BRCA wild-type (BRCAwt) HGSOC patients.

24 he accumulation of HBA metabolites caused by HGSOC was also associated with reduced expression of suc

25 , a chemokine receptor commonly expressed by HGSOC cells.

26 tly reported that Elafin is overexpressed by HGSOC and is associated with poor overall survival.

27 ients with high-grade serous ovarian cancer (HGSOC) and 100 control patients with benign or non-neopl

28 h advanced high-grade serous ovarian cancer (HGSOC) and is associated with drug resistance and a poor

29 notypes of high-grade serous ovarian cancer (HGSOC) and to evaluate CT indicators of cytoreductive ou

30 omen, with high-grade serous ovarian cancer (HGSOC) being the most common and lethal subtype of this

31 genes for high-grade serous ovarian cancer (HGSOC) by performing a transcriptome-wide association st

32 OVSAHO, a high-grade serous ovarian cancer (HGSOC) cell line.

33 pressed in high-grade serous ovarian cancer (HGSOC) cell lines compared with normal cells-ovarian sur

34 simulated high-grade serous ovarian cancer (HGSOC) datasets, smoothed ST slides have better separabi

35 ients with high-grade serous ovarian cancer (HGSOC) from the Australian Ovarian Cancer Study to evalu

36 High grade serous ovarian cancer (HGSOC) is a fatal gynecologic malignancy in the U.S. wit

37 High-grade serous ovarian cancer (HGSOC) is a highly lethal gynecologic malignancy in wome

38 High-grade serous ovarian cancer (HGSOC) is an archetypal cancer of genomic instability(1-

39 High grade serous ovarian cancer (HGSOC) is an exemplar tumour type showing extreme, but p

40 High-grade serous ovarian cancer (HGSOC) is one of the deadliest cancers for women, with a

41 eatment of high-grade serous ovarian cancer (HGSOC) is the development of progressive resistance to p

42 High grade serous ovarian cancer (HGSOC) is the fifth leading cause of cancer deaths among

43 origin for high grade serous ovarian cancer (HGSOC) led to a new perspective on the biology and thera

44 lopment of high-grade serous ovarian cancer (HGSOC) may define the molecular basis of the profound st

45 cated that high-grade serous ovarian cancer (HGSOC) originates in the fallopian tube, where the earli

46 ely 30% of high-grade serous ovarian cancer (HGSOC) patients and is a recurrent lesion in uterine car

47 recurrent high-grade serous ovarian cancer (HGSOC) patients in which we assessed epigenome-wide asso

48 from >100 high-grade serous ovarian cancer (HGSOC) samples, primarily from a phase II clinical trial

49 e of human high-grade serous ovarian cancer (HGSOC) should not only resemble its tumour of origin at

50 nalyses of high-grade serous ovarian cancer (HGSOC) so far have not uncovered potential drug targets,

51 esponse of high grade serous ovarian cancer (HGSOC) to neoadjuvant chemotherapy (NACT).

52 ients with high-grade serous ovarian cancer (HGSOC)(1).

53 High-grade serous ovarian cancer (HGSOC), a high-risk, poor prognosis ovarian cancer subty

54 ients with high grade serous ovarian cancer (HGSOC), addition of the ATR inhibitor berzosertib to gem

55 eatures of high-grade serous ovarian cancer (HGSOC), to assess their associations with time-to-diseas

56 (NACT) in high-grade serous ovarian cancer (HGSOC), we performed immunogenomic analysis of treatment

57 changes in high-grade serous ovarian cancer (HGSOC), we performed whole genome sequencing on a rare c

58 high-grade serous epithelial ovarian cancer (HGSOC).

59 those with high-grade serous ovarian cancer (HGSOC).

60 ostate and high-grade serous ovarian cancer (HGSOC).

61 agement of high grade serous ovarian cancer (HGSOC).

62 rtality in high-grade serous ovarian cancer (HGSOC).

63 laparib in high-grade serous ovarian cancer (HGSOC).

64 ients with high-grade serous ovarian cancer (HGSOC).

65 s from BRCA1/BRCA2-associated breast cancer, HGSOC, and PaC were developed and evaluated for their re

66 Most high grade serous ovarian cancers (HGSOC) originate in the fallopian tube but spread to the

67 High-grade serous ovarian cancers (HGSOC) represent the most common subtype of ovarian mali

68 TIC) into high-grade serous ovarian cancers (HGSOC).

69 High-grade serous ovarian carcinoma (HGSOC) accounts for most ovarian cancer cases, and it is

70 High grade serous ovarian carcinoma (HGSOC) accounts for ~ 70% of ovarian cancer cases.

71 High-grade serous ovarian carcinoma (HGSOC) and basal-like breast cancer (BLBC) share many fe

72 ival of high grade serous ovarian carcinoma (HGSOC) cells by repressing expression of Death Receptors

73 te that high-grade serous ovarian carcinoma (HGSOC) contains distinct immune aggregates with varying

74 High-grade serous ovarian carcinoma (HGSOC) is a cancer with dismal prognosis due to the limi

75 High grade serous ovarian carcinoma (HGSOC) is a highly heterogeneous disease that typically

76 High-grade serous ovarian carcinoma (HGSOC) is a lethal disease for which improved screening

77 High-grade serous ovarian carcinoma (HGSOC) is a molecularly heterogeneous and lethal maligna

78 High-grade serous ovarian carcinoma (HGSOC) is characterised by poor outcome and extreme chro

79 ture of high-grade serous ovarian carcinoma (HGSOC) is frequent amplification of the 3q26 locus harbo

80 High-grade serous ovarian carcinoma (HGSOC) is genetically unstable and characterised by the

81 High-grade serous ovarian carcinoma (HGSOC) is the most aggressive type of ovarian cancer, of

82 High-grade serous ovarian carcinoma (HGSOC) is the most common and aggressive form of epithel

83 High-grade serous ovarian carcinoma (HGSOC) is the most frequent type of ovarian cancer and h

84 High-grade serous ovarian carcinoma (HGSOC) is the most genomically complex cancer, character

85 High-grade serous ovarian carcinoma (HGSOC) is the most lethal gynecologic malignancy in indu

86 High-grade serous ovarian carcinoma (HGSOC) is the most lethal gynecological cancer with few

87 High-grade serous ovarian carcinoma (HGSOC) is the predominant and most lethal form of ovaria

88 igin of high grade serous ovarian carcinoma (HGSOC) remains controversial, with fallopian tube epithe

89 sistant high-grade serous ovarian carcinoma (HGSOC) with measurable and biopsiable disease (cohort 5)

90 ypes of high-grade serous ovarian carcinoma (HGSOC), but their interpretation and translation are com

91 High-grade serous ovarian carcinoma (HGSOC), the deadliest form of ovarian cancer, is typical

92 High-grade serous ovarian carcinoma (HGSOC), the most lethal gynecological cancer, often lead

93 totype, high-grade serous ovarian carcinoma (HGSOC), while p53 mutations are much less frequent in ot

94 ence in high-grade serous ovarian carcinoma (HGSOC), with the loss of the tumour suppressor PTEN in H

95 ture of high-grade serous ovarian carcinoma (HGSOC).

96 ent for high-grade serous ovarian carcinoma (HGSOC).

97 agnosed high-grade serous ovarian carcinoma (HGSOC).

98 ment of high-grade serous ovarian carcinoma (HGSOC).

99 vity is high-grade serous ovarian carcinoma (HGSOC).

100 ity of high-grade serous ovarian carcinomas (HGSOC) provide the necessary context to study the mechan

101 d from high-grade serous ovarian carcinomas (HGSOC), an aggressive cancer characterized by ubiquitous

102 In addition to such genetic changes, HGSOC is characterized by altered metabolism, including

103 hat could improve outcomes in chemoresistant HGSOC.

104 RNA sequencing in pre- and post-chemotherapy HGSOC sample pairs from 11 patients, and in fallopian tu

105 Comparing HGSOC tumors with normal fallopian tube tissues we obser

106 y of homologous recombination (HR)-deficient HGSOC tumors to platinum-based chemotherapy.

107 py in combination with PARPi in HR-deficient HGSOC and also as a single agent for the treatment of re

108 gous recombination (HR) DNA repair-deficient HGSOC-patient-derived xenograft (PDX) in vivo.

109 a therapeutic vulnerability in PTEN-depleted HGSOC.

110 rin signaling pathway as critical to dormant HGSOC cell survival.

111 ly describe the mutational landscape driving HGSOC, exploiting a large (N = 324), deeply whole genome

112 he effects of MRCKA knockdown in established HGSOC cell lines demonstrated that MRCKA was integral to

113 revalent signature consisting of established HGSOC driver kinases, as well as several kinases previou

114 ntiate the immunogenicity of immune-excluded HGSOC tumors.

115 genome-wide association study available for HGSOC (N = 13,037 cases and 40,941 controls).

116 d demonstrates that this is not the case for HGSOC.

117 ng 23 new candidate susceptibility genes for HGSOC.

118 he current gold-standard response marker for HGSOC in blood, as well as to disease volume on computed

119 es consensus molecular subtyping methods for HGSOC, including tools like consensusOV, for accurate ov

120 results comport with a dualistic origin for HGSOC and suggest that the cell-of-origin might influenc

121 issal of discrete transcriptome subtypes for HGSOC and replacement by a more realistic model of conti

122 corporates consensus molecular subtyping for HGSOC.

123 potential of eTreg-focused therapeutics for HGSOC and other HRD-related tumors.

124 ase for breast cancer, endocrine therapy for HGSOC has not shown consistently promising results.

125 ial of colforsin daropate as a treatment for HGSOC.

126 of CXCR4 pathway in expression profiles from HGSOC correlated with enrichment of a mutated TP53 gene

127 had significantly lower mortality rates from HGSOC compared with women with the lowest prediagnosis d

128 ptor expression patterns likely modulate how HGSOC cells interact with their local microenvironment.

129 vivo shRNA screen using an established human HGSOC cell line growing either subcutaneously or intrape

130 nscriptomics and genomics suggest that human HGSOC arises from both cell types.

131 otypically, and genomically similar to human HGSOC.

132 alterations and phenotypes similar to human HGSOC.

133 , we use spatial transcriptomics to identify HGSOC subclones and study their association with infiltr

134 sion more effectively than olaparib alone in HGSOC patient-derived xenograft (PDX) models.

135 first comprehensive metabolomics analysis in HGSOC and propose a new set of metabolites as biomarkers

136 spheroid formation and induced apoptosis in HGSOC cells, suggesting that MRCKA may be a promising th

137 ons are present in pre-treatment biopsies in HGSOC and can undergo expansion during chemotherapy, cau

138 CA in HGSOC may therefore present a potential driver of tumour

139 However, the prevalence of CA in HGSOC, its relationship to genomic biomarkers of CIN and

140 on of p53 aggregation and chemoresistance in HGSOC cells, we further demonstrated that the overexpres

141 that drives stemness and chemoresistance in HGSOC, suggesting that the miR-181a-SFRP4 axis can be ev

142 nce that structural variants (SV) cluster in HGSOC, but are absent in one ultramutated tumor, providi

143 exhibit allele-specific binding for CTCF in HGSOC and normal fallopian tube secretory epithelium cel

144 lethal replication stress and DNA damage in HGSOC, warranting further clinical development.

145 TORi and CHK1i induces greater cell death in HGSOC cells and in vivo models by causing lethal replica

146 ber losses could contribute to HR defects in HGSOC.

147 low OXPHOS and high OXPHOS tumor deposits in HGSOC patients and to detect their differential response

148 Immunotherapies have had limited efficacy in HGSOC(11-13), highlighting an unmet need to assess how m

149 e FTE that is also ubiquitously expressed in HGSOC where it is an important driver of proliferation,

150 n important regulator of ABCC1 expression in HGSOC.

151 Fibroblasts in HGSOC metastases expressed TGFBI and stimulated macropha

152 ate by perturbing expression of each gene in HGSOC precursor cells.

153 BRD4 is the 4th most amplified gene in HGSOC, which correlates with poor patients' prognosis.

154 he high degree of subclonal heterogeneity in HGSOC and suggests that subclone-specific ligand and rec

155 oteins of interest (pSTAT3, HGF, and IL6) in HGSOC samples of origin-based cell lines (OVCAR-8, FTSEC

156 gnostic value with potential implications in HGSOC clinical management.

157 of PI3K and cell-cycle pathway inhibitors in HGSOC.

158 e extracellular matrix and tumor invasion in HGSOC.

159 oss-of-function analysis of these kinases in HGSOC cells indicated MRCKA (also known as CDC42BPA) as

160 , a region with frequent copy number loss in HGSOC, these findings suggest that ZC3H18 copy number lo

161 specific early molecular response marker in HGSOC and warrants further investigation in larger cohor

162 vergence and immune resistance mechanisms in HGSOC.

163 ponent of the metastatic microenvironment in HGSOC.

164 w biomarker-based clinical trials of NACT in HGSOC.

165 tion of the same signaling pathway occurs in HGSOC PDXs that are resistant to poly(ADP-ribose) polyme

166 trate that Netrin-1 and -3 overexpression in HGSOC correlates with poor outcome.

167 uncover disease-outcome-related patterns in HGSOC transcriptomes that may reveal novel drug targets.

168 emergence of subclonal tumour populations in HGSOC was associated with the development of resistant d

169 th the loss of the tumour suppressor PTEN in HGSOC being associated with poor prognosis.

170 ial predictive biomarker of NACT response in HGSOC, which suggests that DKI is a promising clinical t

171 nisms of oncogenesis and therapy response in HGSOC.

172 er to characterize their respective roles in HGSOC development.

173 igh-throughput drug combination screening in HGSOC cells.

174 Functional screens in HGSOC cell lines found evidence of essentiality for thre

175 cytogenetic changes typical of those seen in HGSOC ovarian cancer cell lines and biopsies.

176 family receptors blocks Netrin signaling in HGSOC cells and compromises viability during the dormanc

177 has been a promising therapeutic strategy in HGSOC.

178 ue immune- and cancer cell subpopulations in HGSOC tumor and ascites samples.

179 EAF6 was associated with shorter survival in HGSOC with 1p34.3 amplifications.

180 tment with ceritinib and PARPi synergized in HGSOC cell lines irrespective of HR status, and a combin

181 In addition, PAX8, an important target in HGSOC and a potential miRNA target (from IPA) was epigen

182 kinome has been therapeutically targeted in HGSOC.

183 ial biomarkers and/or therapeutic targets in HGSOC.

184 ned gemcitabine and ATR inhibitor therapy in HGSOC ovarian cancer.

185 for survival after chemotherapy treatment in HGSOC.

186 sable elements remains largely unexplored in HGSOC since conventional short-read sequencing is unable

187 as several kinases previously unexplored in HGSOC.

188 gene expression and splice junction usage in HGSOC-relevant tissue types (N = 2,169) and the largest

189 paclitaxel, the commonest treatment used in HGSOC.

190 bited variable single agent IC(50) values in HGSOC cell lines.

191 5; 95% CI, 1.70-3.23; P < .001) and incident HGSOC (9.4% methylated; HR, 1.93; 95% CI, 1.36-2.73; P <

192 1 methylation and incident TNBC and incident HGSOC were analyzed by Cox proportional hazards regressi

193 ident TNBC and 511 women developing incident HGSOC were matched with cancer-free controls in a nested

194 d in a large proportion of STIC and invasive HGSOC tumors, implicating RNF20/H2Bub1 loss as an early

195 filtrating lymphocytes from freshly isolated HGSOC and NSCLC biopsies.

196 g 34 patients with advanced stage IIIC or IV HGSOC to assess changes in the tumor genome and transcri

197 Armed with this knowledge, HGSOC treatment was revised to include new agents.

198 ersecting regulatory biofeatures at 17 known HGSOC susceptibility loci in FTSECs (P = 3.8 x 10(-30)),

199 Therefore, limiting HGSOC research to modeling based on ovarian surface epit

200 ic analysis of 26 ovarian cancer cell lines, HGSOC tumours, immortalized ovarian surface epithelial c

201 diagnosed with early-stage TNBC or localized HGSOC.

202 o a predominantly epithelial and mesenchymal HGSOC tumour cluster.

203 OSE-derived organoids also caused metastatic HGSOC, although with longer latency and lower penetrance

204 Molecularly, HGSOC shows high degree of genomic instability associate

205 orter PFS for both patients with BRCA-mutant HGSOC (multiple regression: hazard ratio [HR] = 26.7 P <

206 s differed between patients with BRCA-mutant HGSOC and patients with BRCA wild-type HGSOC.

207 me and survival in patients with BRCA-mutant HGSOC and those with BRCA wild-type HGSOC.

208 orter PFS for both patients with BRCA-mutant HGSOC and those with BRCA wild-type HGSOC.

209 uctive outcome for patients with BRCA-mutant HGSOC, presence of PD in lesser sac (odds ratio [OR] = 2

210 In treatment-naive HGSOC, we found that immune-cell-excluded and inflammato

211 f canonical Wnt signaling in treatment-naive HGSOC.

212 mutant forms of p53, which occur in >60% of HGSOC, bind and inhibit ERalpha function and confer resi

213 articularly attractive candidate, as ~70% of HGSOC tumors stain positively for ERalpha and there are

214 laparib therapy, we performed an analysis of HGSOC tumors from three patients without germline BRCA1/

215 In this study, we examined the chronology of HGSOC subtype evolution in the context of these factors

216 tein expression, we identified 5 clusters of HGSOC, which validated across two independent patient co

217 -based biomarkers for the early detection of HGSOC and will contribute to the development of new targ

218 us may be early events in the development of HGSOC, and associated with chromosomal instability.

219 r HOXD9 overexpression reveals enrichment of HGSOC risk variants within HOXD9 target genes (P=6 x 10(

220 Lkb1) resulted in successfully generation of HGSOC, albeit with different latencies and pathophysiolo

221 The heterogeneity of HGSOC, including few shared oncogenic drivers and origin

222 ctrometry, we mapped the kinome landscape of HGSOC tumors from patients and patient-derived xenograft

223 A vast majority of HGSOC are diagnosed at the late stage of the disease whe

224 zygous loss of RNF20 defines the majority of HGSOC tumors.

225 the need for a fallopian tube-based model of HGSOC, we have developed a system for studying human fal

226 ll as in clinically relevant mouse models of HGSOC post-platinum therapy.

227 human tumours indicates a possible origin of HGSOC either from the fallopian tube or from the ovarian

228 demonstrated that in a unique population of HGSOC cancer cells with cancer stem cell properties, p53

229 fallopian tube cancers may be precursors of HGSOC but evolutionary evidence for this hypothesis has

230 gesting both cell types may be precursors of HGSOC.

231 hat drive the development and progression of HGSOC.

232 reviously inaccessible repetitive regions of HGSOC, including centromeric and transposable element hy

233 esent a framework to predict the response of HGSOC patients to NACT integrating baseline clinical, bl

234 rstand the poor chemoresponse of a subset of HGSOC patients and suggest p53 aggregation as a new mark

235 d immunoreactive and mesenchymal subtypes of HGSOC, which have prognostic implications, reflect the a

236 s study suggests that molecular subtyping of HGSOC based on HR status and RB1 expression may provide

237 opment and mediate genetic susceptibility of HGSOC.

238 sing therapeutic target for the treatment of HGSOC.

239 reas is impeded by our poor understanding of HGSOC pathogenesis.

240 X1778 treatment of platinum-resistant OVCAR3 HGSOC mouse xenografts abrogated tumor growth without ob

241 By fitting to individual patient HGSOC data, our models successfully capture the dynamics

242 Colforsin daropate also prevented HGSOC cells from invading ovarian surface epithelial cel

243 r, in patient-derived xenografts and primary HGSOC tumors, ZC3H18 and E2F4 mRNA levels are positively

244 amples, including three ascites, two primary HGSOC tumors and three patient ascites-derived xenograft

245 Disturbed pathways in BMs versus primary HGSOC constituted a complex network and included the cel

246 well as hippo signaling in normal vs primary HGSOC; valine, leucine, and isoleucine degradation and e

247 als the core archetypes found in progressive HGSOC and shows consistent enrichment of subclones with

248 l series of primary and metastatic/recurrent HGSOC cases.

249 Subclonality of recurrent HGSOC alterations was evident for proliferative tumors,

250 tion and endocytosis in primary vs recurrent HGSOC; and pathways containing immune driver genes in op

251 xpression signatures in primary and relapsed HGSOC.

252 ctivate ERalpha-SP1 target genes and renders HGSOC markedly more sensitive to endocrine therapy.

253 the antibody based therapy for Pt-resistant HGSOC cell lines.

254 elapse from patients with platinum-sensitive HGSOC recurrence who were treated > 5 years with olapari

255 esis inhibitor GMX1778 strikingly sensitized HGSOC cells to JW-98 treatment.

256 s the potential of deep learning to simplify HGSOC triage and improve early treatment planning by acc

257 ll lines (OVCAR-8, FTSEC) and in early-stage HGSOC patient serum exosome samples using LC/MS-MS and p

258 ghting translational potential in late-stage HGSOC, combined JW-98/GMX1778 treatment of platinum-resi

259 insights into the pathogenesis of low stage HGSOC.

260 In summary, HGSOC PDO cultures provide validated genomic models for

261 ells was necessary and sufficient to support HGSOC proliferation, adhesion, migration, and invasion.

262 resistance, metastasis, and recurrence than HGSOC.

263 cer research is based on the hypothesis that HGSOC arises from ovarian surface epithelial cells.

264 It has been shown that HGSOC subtype II epithelial ovarian cancer accounts for

265 To comprehensively characterize the HGSOC ascites ecosystem, we used single-cell RNA sequenc

266 NBC group and 3493 cases and controls in the HGSOC group, respectively, 7 (0.3%) and 3 (0.1%) were Am

267 Here, we report that the HGSOC tumor-mesothelial niche was hypoxic, and hypoxic s

268 or this network in genetic susceptibility to HGSOC.

269 sed on signaling pathways that are unique to HGSOC, both of which could improve the outcome for women

270 veloped as an effective drug target to treat HGSOC derived from both the OSE and FTE.

271 ombined with conventional therapies to treat HGSOC.

272 e with established peritoneal disease in two HGSOC syngeneic models and progression-free survival in

273 f incomplete cytoreduction in BRCA wild-type HGSOC (multiple regression: P < .001 each CT feature).

274 26.7 P < .001) and those with BRCA wild-type HGSOC (univariate analysis: reader 1, HR = 2.42, P < .00

275 with BRCA mutant and 75 with BRCA wild-type HGSOC) who underwent CT before primary debulking.

276 A-mutant HGSOC and those with BRCA wild-type HGSOC.

277 A-mutant HGSOC and those with BRCA wild-type HGSOC.

278 utant HGSOC and patients with BRCA wild-type HGSOC.

279 Here we utilized HGSOC cell lines and patient-derived xenografts (PDXs) t

280 on of tumor suppressor genes associated with HGSOC in two different combinations (Brca1, Tp53, Pten w

281 L associations at 47 regions associated with HGSOC risk (P</=10(-5)).

282 Genomic lesions associated with HGSOC subtypes tended to be subclonal, implying subtype

283 ation of expression patterns correlated with HGSOC, we performed weighted gene co-expression network

284 t retrospective analysis of 92 patients with HGSOC (median age, 61 years) with abdominopelvic CT befo

285 assay in 34 serum samples from patients with HGSOC and 36 healthy women.

286 g this approach, we studied 18 patients with HGSOC over a multi-year period from diagnosis to recurre

287 outine clinical visits from 40 patients with HGSOC undergoing heterogeneous standard of care treatmen

288 Seventeen patients with HGSOC were imaged at 3 T and had biopsy samples taken pr

289 ally separated samples from 14 patients with HGSOC who received platinum-based chemotherapy.

290 LOVAR subtypes and survival in patients with HGSOC.

291 m 22 ascites specimens from 11 patients with HGSOC.

292 sites from 42 treatment-naive patients with HGSOC.

293 ociated with poor prognosis in patients with HGSOC.

294 of peritoneal fluid samples from women with HGSOC (frequency as low as 1 mutant per 24,736 normal ge

295 17 peritoneal fluid samples from women with HGSOC and 20 from women without cancer.

296 ease at the start of treatment in women with HGSOC and that a decrease of </=60% in TP53MAF after one

297 However, among 325 women with HGSOC, better adherence to HEI-2020 was associated with

298 efore cytoreductive surgery in 46 women with HGSOC, whose tumors were subjected to molecular analysis

299 ich could improve the outcome for women with HGSOC.

300 Within HGSOC, 57 probes highlighting 17 genes displayed signifi