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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
37 FRalpha), which is expressed widely on human ovarian tumors, along with a syngeneic rat tumor model e
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
42 ing expression of miRNAs and mRNAs in serous ovarian tumors and cell lines and normal ovarian surface
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
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
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
75 ed tissue microarrays, one containing benign ovarian tumors, borderline/low malignant potential (LMP)
79 essed in metastases and advanced-stage human ovarian tumors but not in normal ovarian epithelium.
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,
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
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
98 erize a self-renewing subpopulation of human ovarian tumor cells (ovarian cancer-initiating cells, OC
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
107 , a stem cell regulatory factor expressed in ovarian tumor cells and vasculature, regulates ALDH(+) o
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
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
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
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
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
149 tinguishable disease, patients with advanced ovarian tumors display a broad range of survival end poi
152 Here, we demonstrate that the deubiquitinase ovarian tumor domain containing ubiquitin aldehyde bindi
155 PLP2 was also proposed to belong to the ovarian tumor domain-containing superfamily of deubiquit
159 se to cps treatment of the immunosuppressive ovarian tumor environment, CD11c(+) cells regained the a
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
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
176 have previously shown that human epithelial ovarian tumors have increased levels of Cox-1, but not C
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
186 onducted genomic analyses of intraperitoneal ovarian tumors in which adaptive resistance to anti-VEGF
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.
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
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
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
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
213 In contrast, we found that mutations in ovarian tumor (otu) interfere with both Sxl germline fun
216 hly conserved deubiquitinating enzyme of the ovarian tumor (otubain) family, whose function has yet t
218 ociated with an increased risk of borderline ovarian tumors, particularly among women who had had mul
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
228 omentum tissue that promote endometrial and ovarian tumor proliferation, migration, and drug resista
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.
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
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
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
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
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
266 these data suggest that LPA initiates EMT in ovarian tumors through beta1-integrin-dependent activati
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.
274 emistry-based cytotoxic modality, sensitizes ovarian tumors to platinum agents and biologics and has
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
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
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
289 imental findings, patient-derived epithelial ovarian tumors with low KLF6 and high KLF6-SV1 expressio
293 umor tissues, such as germ cell, breast, and ovarian tumors, with in the latter case, evidence for a
295 tumor efficacy when dosed orally in an A2780 ovarian tumor xenograft model (TGI of 97% was observed o
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
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