コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 in acquired resistance to platinum drugs in ovarian cancer.
2 by mutated TP53, a gene commonly altered in ovarian cancer.
3 atinum-sensitive, relapsed high-grade serous ovarian cancer.
4 es in patients with suspected advanced-stage ovarian cancer.
5 M expression and reduced overall survival in ovarian cancer.
6 s (CAFs) contribute to the poor prognosis of ovarian cancer.
7 nvasive end-of-life care among patients with ovarian cancer.
8 intrabursal mouse xenograft models of human ovarian cancer.
9 logical function of IL-6R mRNA expression in ovarian cancer.
10 R) DNA repair genes are linked to breast and ovarian cancer.
11 inical trials in patients with leukaemia and ovarian cancer.
12 des a therapeutic strategy for highly lethal ovarian cancer.
13 urvival and chemoresistance in patients with ovarian cancer.
14 r use in liposomal form for the treatment of ovarian cancer.
15 nts with high grade but not low grade serous ovarian cancer.
16 ted with 10 kilobase tandem duplications in ovarian cancer.
17 n of CS-E, which is a possible biomarker for ovarian cancer.
18 n tissue phantoms and in an in vivo model of ovarian cancer.
19 le-appearing cysts were given a diagnosis of ovarian cancer.
20 CA2 severely increase the risk of breast and ovarian cancer.
21 variant carriers have an increased risk for ovarian cancer.
22 mation and development of drug resistance in ovarian cancer.
23 detect sentinel nodes (SNs) in patients with ovarian cancer.
24 tly is the best serum-based tumor marker for ovarian cancer.
25 of metastatic hepatic involvement in serous ovarian cancer.
26 e Ciota (PKCiota) is an oncogene in lung and ovarian cancer.
27 ties in end-of-life care among patients with ovarian cancer.
28 with FRalpha-positive and platinum-resistant ovarian cancer.
29 hich indicates its therapeutic potential for ovarian cancer.
30 years) or a family history of breast and/or ovarian cancer.
31 ve been identified as potent EMT inducers in ovarian cancer.
32 that UBR5 can confer cisplatin resistance in ovarian cancer.
33 n patients with platinum-sensitive recurrent ovarian cancer.
34 underlying platinum and taxane resistance in ovarian cancer.
35 rring, growth-promoting mutational events in ovarian cancer.
36 a cell-line xenograft model of disseminated ovarian cancer.
37 and human myeloid dendritic cells (TIDC) in ovarian cancer.
38 nt and treatment of patients with breast and ovarian cancer.
39 target genes for future treatment efforts in ovarian cancer.
40 berrations responsible for poor prognosis in ovarian cancer.
41 LPP enhances the efficacy of chemotherapy in ovarian cancer.
42 trend = 0.01) were inversely associated with ovarian cancer.
43 eatic adenocarcinoma and advanced epithelial ovarian cancer.
44 sible role of tumoral expression of IL-6R in ovarian cancer.
45 reclinical models of advanced pancreatic and ovarian cancer.
46 serum biomarker and a therapeutic target for ovarian cancer.
47 as a novel therapeutic target for resistant ovarian cancer.
48 d may provide a new therapeutic strategy for ovarian cancer.
49 olvement of this gene in the commencement of ovarian cancers.
50 ated in many colorectal, hepatocellular, and ovarian cancers.
51 ognosis and treatment response in breast and ovarian cancers.
52 orse overall survival in breast, uterine and ovarian cancers.
53 onsortium (OCAC), including 9,162 women with ovarian cancers, 2,354 women with borderline tumors, and
54 curacy for the screening pelvic examination: ovarian cancer (4 studies; n = 26432), bacterial vaginos
56 ation between PID and the risk of epithelial ovarian cancer according to tumor behavior and histotype
58 In an established mouse xenograft model of ovarian cancer, adoptive transfer of NK cells conditione
59 %, 1.0%) of 2763 patients were found to have ovarian cancer after an average follow-up of 5.1 years +
60 nificant prognostic value in both breast and ovarian cancers after considering established clinical v
62 125 (CA-125), interpreted using the risk of ovarian cancer algorithm (ROCA), and transvaginal sonogr
63 rescent dyes to mice bearing intraperitoneal ovarian cancer allowed visualization of tumor-associated
64 38 years; IQR, 31-47 years) eligible for the ovarian cancer analysis, and 2213 women (median age, 47
66 d agents currently used to treat BRCA-mutant ovarian cancer and are in clinical trials for other canc
67 llected from patients with colon, breast, or ovarian cancer and cell lines harboring specific oncogen
68 fectiveness of HDAC inhibitors when treating ovarian cancer and other solid tumors characterized by i
70 erved in gastrointestinal, lung, breast, and ovarian cancer and this could decrease the threshold req
71 tromal and tumour compartments of aggressive ovarian cancers and its levels correlate with poor clini
73 were diagnosed with breast cancer, 109 with ovarian cancer, and 245 with contralateral breast cancer
74 with a focus on melanoma, and pancreatic and ovarian cancer, and discuss how scientific advances may
75 K2) is highly expressed in high-grade serous ovarian cancer, and we investigated its role in Akt acti
76 al differences between serous and non-serous ovarian cancers, and further distinguish different non-s
77 f benign sources has unveiled a multitude of ovarian cancer antigens (MUC16, MSLN, LGALS1, IDO1, KLK1
80 helicase is linked to hereditary breast and ovarian cancers as well as bone marrow failure disorder
81 studies have reported decreased incidence of ovarian cancer associated with regular intake of NSAIDs,
82 s, conducted between 1989 and 2009, from the Ovarian Cancer Association Consortium (OCAC), including
93 cell death and DNA damage was studied in two ovarian cancer cell lines (OVCAR3 and A2780), normal ham
94 ow that MICU1 is overexpressed in a panel of ovarian cancer cell lines and that MICU1 overexpression
96 MGCR), was found to be over-expressed in all ovarian cancer cell lines examined and upregulated by mu
97 portantly, we found that cisplatin-resistant ovarian cancer cell lines exhibit lower levels of MOAP-1
99 ing of 13 established and 12 patient derived ovarian cancer cell lines revealed significant bioenerge
100 y against cisplatin-resistant A2780Cis human ovarian cancer cells (IC50 74 muM, blue light) with a ph
101 tified Nectin-4 shedding from the surface of ovarian cancer cells after stimulation with lysophosphat
103 rate that metastasis-associated behaviors of ovarian cancer cells and MCAs are influenced by cellular
104 d platinum-sensitive and platinum- resistant ovarian cancer cells and ovarian cancer stem cells and (
105 9), which is upregulated in human breast and ovarian cancer cells and released from apoptotic tumor c
107 l that EMT can be induced in epithelial-like ovarian cancer cells by co-expressing constitutively act
108 find that ARID1B knockdown in ARID1A mutant ovarian cancer cells causes similar loss of enhancer arc
111 we showed that acquired cisplatin-resistant ovarian cancer cells expressed high levels of MKP-1 and
114 pithelial-to-mesenchymal transition (EMT) of ovarian cancer cells in vivo, STAT4 failed to induce EMT
119 gulation of metastasis-associated behaviors, ovarian cancer cells that express low endogenous levels
120 s and reverses multi-drug resistance against ovarian cancer cells through downregulation of survivin.
122 Depleting or inhibiting USP13 sensitizes ovarian cancer cells to cisplatin and PARP inhibitor (ol
124 how inhibiting DNA methylation can sensitize ovarian cancer cells to platinum drugs, in large part by
125 itaxel (PTX) and doxorubicin (DOX) resistant ovarian cancer cells to PTX and DOX by inhibiting surviv
129 st of mesenchymal traits in mesenchymal-like ovarian cancer cells, whereas expressing constitutively
130 its clonal growth, migration and invasion of ovarian cancer cells, whereas silencing in vivo inhibits
131 is and suppressing migration and invasion in ovarian cancer cells, which indicates its therapeutic po
140 C transcriptomic profiles (Classification of Ovarian Cancer [CLOVAR]), and to develop an imaging-base
141 ysis of 7 nested case-control studies in the Ovarian Cancer Cohort Consortium to investigate the asso
142 0 scores, were associated with lower risk of ovarian cancer (comparing the highest quartile (4th) vs.
143 cancer screening studies, low prevalence of ovarian cancer consistently resulted in low positive pre
144 try-Medicare data, we assessed patients with ovarian cancer deceased in 2000 to 2012 with at least 13
146 I-MS as a powerful approach for rapid serous ovarian cancer diagnosis based on altered metabolic sign
150 Despite clinical remission of epithelial ovarian cancer (EOC) after surgical resection and first-
160 ociation between hysterectomy and epithelial ovarian cancer (EOC) was considered well established, in
161 e with prognosis in patients with epithelial ovarian cancer (EOC), but their prognostic importance an
164 ngiogenesis) inhibitors such as pazopanib in ovarian cancer even when (18)F-FDG PET/CT does not indic
166 ue microarray analysis revealed that >98% of ovarian cancers express the prolactin receptor (PRLR), f
167 rd of care for women with platinum-sensitive ovarian cancer following a complete or partial response
168 evel, we integrated protein and mRNA data of ovarian cancer from The Cancer Genome Atlas (TCGA) and C
169 Furthermore, UBR5 expression was higher in ovarian cancers from cisplatin-resistant patients than f
176 inhibit certain tumor cell lines, including ovarian cancer, hepatocarcinoma and retinoblastoma, thro
177 ovarian and other cancers.High-grade serous ovarian cancers (HGS-OvCa) frequently develop chemothera
178 fective chemotherapies for high-grade serous ovarian cancers (HGS-OvCa) has motivated a search for al
179 mutations in patients with high-grade serous ovarian cancer (HGSC) are associated with favorable resp
182 ed in approximately 30% of high-grade serous ovarian cancer (HGSOC) patients and is a recurrent lesio
183 y (CT) imaging features of high-grade serous ovarian cancer (HGSOC), to assess their associations wit
189 endometrial cancer in 83 (30%) of 279 women; ovarian cancer in 28 (10%) of 279 women; and colorectal
190 formed at the Center for Familial Breast and Ovarian Cancer in Cologne, Germany; data analysis, Novem
191 outcomes in platinum-resistant and recurrent ovarian cancer in part by effects on DNA repair and anti
192 by identifying patients with advanced-stage ovarian cancer in whom > 1 cm of residual disease will b
202 d that ID8, a widely-used syngeneic model of ovarian cancer, lacked any of the frequent mutations in
203 d BRCA2 mutations are frequent in women with ovarian cancer, many such women have not been tested, es
204 4 patients with pathologically proven serous ovarian cancer (mean age +/- standard deviation, 59 year
206 ential key transcription factors involved in ovarian cancer metastasis and identified STAT4 as a crit
207 tudy established a model that STAT4 promotes ovarian cancer metastasis via tumor-derived Wnt7a-induce
210 nstrate the visualization of intraperitoneal ovarian cancer micrometastasis as small as 100 mum with
214 ere we report an integrated analysis of >700 ovarian cancer molecular profiles, including genomic dat
215 end = 0.002) and a positive association with ovarian cancer mortality (HR, 1.31 [CI, 1.07 to 1.61]; P
216 ra-red fluorescence (NIRF) imaging on SKOV-3 ovarian cancer mouse model demonstrated that the NIR dye
218 pecifically to N-glycans present on 11 of 19 ovarian cancer (OC) and 8 of 14 breast cancer cell lines
220 l sonography (TVS) for women at high risk of ovarian cancer (OC) or fallopian tube cancer (FTC).
221 ant risk genes for breast cancer (BC) and/or ovarian cancer (OC), including BRCA1 and BRCA2, explain
223 the mutation landscape of serous epithelial ovarian cancer, other non-serous subtypes of the disease
225 e investigated its role in Akt activation in ovarian cancer (OVCa) cell lines (OVCAR-3, SKOV-3, and C
227 er Genome Atlas mRNA expression data for HGS ovarian cancer patient samples, we observed that six enz
228 use of targeted PARP-inhibitor therapies in ovarian cancer patients carrying deleterious missense RA
230 ce treatment in platinum-sensitive, relapsed ovarian cancer patients with a BRCA1/2 mutation who had
231 sh UBC as a promising therapeutic target for ovarian cancer patients with recurrent UBB silencing.
232 In matched samples from 11 high-grade serous ovarian cancer patients, we detected 2-20-fold more sN4
236 e personalized care and survival outcomes of ovarian cancer patients.Significance: Epigenomic targeti
238 tanding the function of Nectin-4 shedding in ovarian cancer progression is critical to facilitate its
239 r pathways/transcription factors involved in ovarian cancer progression, poor clinical outcome, and c
242 an abnormal screening pelvic examination for ovarian cancer ranged from 5% to 36% at 1 year, with the
244 ublets are a standard of care for women with ovarian cancer recurring 6 months after completion of in
249 n overall healthy dietary pattern may reduce ovarian cancer risk in African-American women, and parti
251 iation with PID, the association of PID with ovarian cancer risk is still somewhat uncertain and requ
252 No association was observed between PID and ovarian cancer risk overall (pOR = 0.99, 95% CI: 0.83, 1
254 een quartiles of dietary quality indices and ovarian cancer risk, adjusting for potential confounders
255 metabolic pathway were overexpressed in HGS ovarian cancer samples compared with normal ovary sample
257 s) and 80,672 Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (PLCO) ever-smoking parti
258 ut the PLCO (Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial) found no reduction.
260 formation of PGCCs and dedifferentiation in ovarian cancer specimens from patients treated with chem
261 ly increased levels of unsaturated lipids in ovarian cancer stem cells (CSCs) as compared to non-CSCs
262 platinum- resistant ovarian cancer cells and ovarian cancer stem cells and (ii) downregulation of bet
263 latinum therapy and was effective in killing ovarian cancer stem cells that contribute to both platin
264 demethylase KDM3A as a critical regulator of ovarian cancer stemness and cisplatin resistance by indu
265 logical meaningful processes associated with ovarian cancer, such as CCL11, CCL16, CCL18, CCL23, CCL8
270 ition to providing a potential biomarker for ovarian cancer, this approach is generally applicable to
271 racellular iron reduces the proliferation of ovarian cancer TICs in vitro, and inhibits both tumor gr
273 copy, can serve as indicators of response in ovarian cancer to multityrosine kinase inhibitor pazopan
274 uppressive microenvironment, and response of ovarian cancers to immune therapies has thus far been di
275 nal case of a patient with high-grade serous ovarian cancer, treated with multiple chemotherapy regim
276 NP(BTZ-DOX) exhibited significantly improved ovarian cancer treatment in SKOV-3 xenograft mouse model
280 thyl transferase 1 (SHMT1) was necessary for ovarian cancer tumor growth and cell migration in cultur
281 ve analysis of the metabolic requirements of ovarian cancer tumor growth has not been performed.
284 -omics profiles of primary high-grade serous ovarian cancer tumours (N=357) to delineate mechanisms u
288 results showed that mRNA levels of IL-6R in ovarian cancer was positively associated with better pro
289 ment of drug resistance in high-grade serous ovarian cancer, were examined from patient derived malig
290 subset of common types of cancer, including ovarian cancer, where NAPRT expression correlates with a
291 l opportunity to identify driver patterns in ovarian cancer, which will acquire some novel and clinic
292 survival in patients with platinum-sensitive ovarian cancer who had achieved a response to platinum-b
295 e-associated colorectal, endometrial, and/or ovarian cancers whose medical records were included in t
296 nalysis on the results for high-grade serous ovarian cancer with the results from analysis of 31,448
298 In a luciferase-expressing ES-2 (ES-2-luc) ovarian cancer xenograft model, single i.p. injections o
299 analyzed 12 treatment groups in trial on an ovarian cancer xenograft, reproducing current therapeuti
WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。