ライフサイエンスコーパス: bladder cancer

1 s (>95th percentile vs.<25th percentile) and bladder cancer.

2 ly diagnosed with muscle-invasive urothelial bladder cancer.

3 nd identify candidate therapeutic targets in bladder cancer.

4 d survival in patients with locally advanced bladder cancer.

5 l analysis of non-muscle invasive urothelial bladder cancer.

6 ese novel genetic associations with risk for bladder cancer.

7 and nitrite intakes were not associated with bladder cancer.

8 multiple oncological conditions, especially bladder cancer.

9 as a novel downstream target of macroH2A1 in bladder cancer.

10 N+) predict poor prognosis in patients with bladder cancer.

11 pact of targeted treatment in the setting of bladder cancer.

12 rently under investigation for patients with bladder cancer.

13 invasion of the perivesical fatty tissue in bladder cancer.

14 on the chemically associated development of bladder cancer.

15 namely SLC14A1, APOBEC3A, PSCA and MYC, with bladder cancer.

16 ess through two main progression pathways in bladder cancer.

17 range, 0.2-13.2 years) and 1261 had incident bladder cancer.

18 ve or adjunct to cystoscopy for diagnosis of bladder cancer.

19 Vysion probes, originally designed to detect bladder cancer.

20 e for ARF in modulating the drug response of bladder cancer.

21 nd applied for a urine metabolomics study of bladder cancer.

22 es have been evaluated for the first time in bladder cancer.

23 (HAase) was reported as a urinary marker of bladder cancer.

24 uggesting an approach to management of human bladder cancer.

25 he first GWAS signal specific for aggressive bladder cancer.

26 ate as a potential new therapeutic target in bladder cancer.

27 nagement of patients with nonmuscle invasive bladder cancer.

28 cant impact on the survival of patients with bladder cancer.

29 an association between swimming pool use and bladder cancer.

30 in consultation for management of recurrent bladder cancer.

31 eatment of advanced human cancers, including bladder cancer.

32 er discovery or chemoradiation strategies in bladder cancer.

33 r PPARG as a candidate therapeutic target in bladder cancer.

34 tegrated analysis of non-invasive (stage Ta) bladder cancer.

35 y used as adjunctive therapy for superficial bladder cancer.

36 n, supporting PPARs as targetable drivers of bladder cancer.

37 icantly associated with an increased risk of bladder cancer.

38 tic drug pioglitazone increases the risk for bladder cancer.

39 2 signaling, which may be applicable in most bladder cancers.

40 ot mutation (S427F/Y) drives 20-25% of human bladder cancers.

41 ch identified FOXA1 mutations in a subset of bladder cancers.

42 treatment for ovarian, prostate, colon, and bladder cancers.

43 d to a specific gene expression signature in bladder cancers.

44 We analyzed 531 Dutch patients with bladder cancer (1990-2012) with information on 7 prespec

45 protein concentrations between patients with bladder cancer (29-344ngmL(-1)) and those with hernia (0

46 305) potently inhibited the proliferation of bladder cancer 5637 cells in a dose- and time-dependent

47 A subset of patients with cN+ bladder cancer achieves long-term survival.

48 icantly associated with an increased risk of bladder cancer [adjusted odds ratios (OR) = 3.90, 95% co

49 cancers combined (renal pelvis, ureter, and bladder cancers: adjusted IRR 2.2, 95% CI 0.9-5.4; N = 8

50 statistically significant increased risk of bladder cancer, although an increased risk, as previousl

51 Nitrate from drinking water and diet and bladder cancer among postmenopausal women in Iowa.

52 ter was associated with an increased risk of bladder cancer among postmenopausal women.

53 We identified incident bladder cancers among a cohort of 34,708 postmenopausal

54 n by-products that have been associated with bladder cancer and adverse birth outcomes.

55 EMP1), as being highly expressed in T2 vs T1 bladder cancer and aggressive vs indolent disease.

56 ss a substantial proportion of patients with bladder cancer and are subject to false-positive results

57 thelial carcinoma is the most common type of bladder cancer and can be categorized as either non-musc

58 e risk of developing certain cancers such as bladder cancer and cervical cancer.

59 icability in case studies of muscle-invasive bladder cancer and essential thrombocythemia.

60 iferation of STAG2 mutated but not wild-type bladder cancer and Ewing sarcoma cell lines.

61 erall survival in four patient datasets from bladder cancer and five patient datasets from colorectal

62 ndorses the guideline on MIBC and metastatic bladder cancer and has added qualifying statements, incl

63 We found no evidence of an association for bladder cancer and hours of swimming pool use.

64 stic and treatment options for patients with bladder cancer and improving our ability to select patie

65 ion with S. haematobium has been linked with bladder cancer and increased risk for HIV infection.

66 evidence for an association between milk and bladder cancer and insufficient evidence for other cance

67 s suggests that ASS1 loss occurs in invasive bladder cancer and is targetable by ADI-PEG 20.

68 in non-invasive than that in muscle-invasive bladder cancer and suggest that cohesin complex-independ

69 re involved in various molecular subtypes of bladder cancer and they sensitize the uroprogenitor cell

70 We evaluated the relationship between bladder cancer and total, chlorinated, and brominated tr

71 mediate, were present in high-grade invasive bladder cancers and associated with more frequent recurr

72 P peptide offers improved early diagnosis of bladder cancers and may also enable new treatment altern

73 ol for predicting the recurrence/clearing of bladder cancer, and for screening undiagnosed individual

74 table for the study of molecular subtypes in bladder cancer, and furthermore indicates a cooperative

75 responses already reported in renal cancer, bladder cancer, and Hodgkin's lymphoma among many others

76 Trials in nonmuscle-invasive bladder cancer are evaluating the role of immunotherapy

77 Most preclinical models for the study of bladder cancer are more appropriate for the study of adv

78 Bladder cancers are a leading cause of death from malign

79 Most bladder cancers are chemically induced, with tobacco smo

80 The majority of bladder cancers are non-muscle-invasive at presentation;

81 squamous cell carcinoma subtypes of invasive bladder cancer, as well as in T24, J82, and UM-UC-3 but

82 We investigated the selenium-bladder cancer association in subjects from Maine, New H

83 nding association of smoking in the selenium-bladder cancer association.

84 Using bladder cancer (BC) as a model, we found that CD14-high

85 on making in cancer care, but its impact for bladder cancer (BC) has not been documented.

86 Bladder cancer (BC) is a common disease.

87 nduce MDSC accumulation and expansion in the bladder cancer (BC) microenvironment via CXCL2/MIF-CXCR2

88 treatment failure and mortality of advanced bladder cancer (BC).

89 may also play critical roles in controlling bladder cancer (BC).

90 Here, we sequenced the exomes of 25 bladder cancer (BCa) cell lines and compared mutations,

91 Data analysis suggested bladder cancer (BCa) was significantly associated with f

92 teins identified as potential biomarkers for bladder cancer by analyzing urine glycoproteins from bla

93 CCLE), guided by genomic characterization of bladder cancer by The Cancer Genome Atlas (TCGA).

94 ccessful ex vivo endoscopic imaging of human bladder cancer by topical (i.e. intravesical) administra

95 Recurrence of bladder cancer can occur repeatedly in the same patient

96 ew Hampshire, and Vermont in the New England Bladder Cancer Case-Control Study.

97 ared with non-muscle-invasive (Ta, T1 stage) bladder cancer (case-case P </= 0.02 for both rs62185668

98 ed in these two regions for a subset of 5551 bladder cancer cases and 10 242 controls.

99 dent replication study using a total of 1131 bladder cancer cases and 12 558 non-cancer controls of J

100 We identified 258 bladder cancer cases, including 130 among women > 10 yea

101 han biomarkers alone but missed about 10% of bladder cancer cases.

102 Our results suggest that TGF-beta can induce bladder cancer cell invasion via mTORC2 signaling, which

103 In contrast, a bladder cancer cell line cotreated with ATM and replicat

104 Chemotaxis assay revealed that bladder cancer cell line J82 induced MDSC migration via

105 Therefore, four human bladder cancer cell lines (with distinct malignancy degr

106 related with the invasive ability of several bladder cancer cell lines and modulation of fibulin-3 ex

107 A subset of bladder cancer cell lines exhibit in vivo histomorpholog

108 To address this limitation, we classified bladder cancer cell lines into molecular subtypes using

109 mortalized normal human urothelial (NHU) and bladder cancer cell lines to agents that disrupt the DNA

110 This identified a panel of bladder cancer cell lines which exhibit genetic alterati

111 ced by treatment with a DNA-damaging drug in bladder cancer cell lines, and APOBEC3A expression was i

112 icant cell death of cervical, colorectal and bladder cancer cell lines, and, importantly, a cisplatin

113 combination in eight distinct chemoresistant bladder cancer cell lines.

114 and apoptosis were analysed in hTERT-NHU and bladder cancer cell lines.

115 osensor response for two different grades of bladder cancer cell lysates.

116 cin complex 2 (mTORC2) as a key regulator of bladder cancer cell migration and invasion, although ups

117 - and SMAD4-independent manner and increased bladder cancer cell migration in a modified scratch woun

118 ancer cells, could regulate mTORC2-dependent bladder cancer cell motility and invasion.

119 rst time revealed that simvastatin inhibited bladder cancer cell proliferation and induced cell cycle

120 ial cells is involved in the interactions of bladder cancer cells (BCs) with the endothelium.

121 dentified pervasive transcriptome changes of bladder cancer cells after treatment with 5-Aza-CdR, and

122 dium of T24 vs. its metastatic subclone T24M bladder cancer cells allowed the identification of 253,

123 L depletion reduced CD24 expression in human bladder cancer cells and blocked cell proliferation in v

124 resulting in reduced levels of DNA repair in bladder cancer cells and radiosensitization.

125 ve examined their anticancer activity in T24 bladder cancer cells bearing mutant HRAS and in T24 xeno

126 Fibulin-3 knockdown in bladder cancer cells decreased the incidence of MIBCs in

127 ly, CRISPR/Cas9-mediated knockout of CDH1 in bladder cancer cells enhanced cell migration.

128 The knockdown of macroH2A1 in bladder cancer cells increased tumorigenicity, radioresi

129 candidate TumiD targets in T24 human urinary bladder cancer cells is augmented by UPF1.

130 as simple and low-cost means of maintaining bladder cancer cells over extended periods of times in o

131 mponents was detected in invasive high-grade bladder cancer cells that expressed Vimentin and lacked

132 ion to drive transdifferentiation of a basal bladder cancer cells to a luminial phenotype.

133 hich can function as a promotility factor in bladder cancer cells, could regulate mTORC2-dependent bl

134 Using bladder cancer cells, we determined that the NOTCH pathw

135 e regulation of stem-like characteristics of bladder cancer cells.

136 tumors in some mice implanted with the MB49 bladder cancer cells.

137 1 knockdown promotes stem-like properties of bladder cancer cells.

138 e context of RXRA/PPAR heterodimers in human bladder cancer cells.

139 the effects of AURKA overexpression in human bladder cancer cells.

140 , inhibited proliferation of PPARG-activated bladder cancer cells.

141 omprehensive analysis of 412 muscle-invasive bladder cancers characterized by multiple TCGA analytica

142 from patients treated in a multidisciplinary bladder cancer clinic (MDBCC) from 2008 to 2013 were rev

143 ung squamous, head and neck, and a subset of bladder cancers coalesced into one subtype typified by T

144 A bladder cancer cohort followed 193,099 persons aged 40 y

145 Among 193,099 persons in the bladder cancer cohort, 34,181 (18%) received pioglitazon

146 Adjusted ORs for bladder cancer comparing participants with exposure abov

147 regions, pioglitazone increased the risk for bladder cancer could be found in European population, an

148 s of outcomes and prognostic factors in HGT1 bladder cancer, deep lamina propria invasion had the lar

149 mplicate AURKA as an effective biomarker for bladder cancer detection as well as therapeutic target e

150 y or other urine-based molecular markers for bladder cancer detection in the initial evaluation of he

151 le for ATDC as a robust pathogenic driver of bladder cancer development, identified downstream effect

152 e mouse urothelium is sufficient to initiate bladder cancer development.

153 As well as detecting the known bladder cancer driver mutations, we report the identific

154 e nuclear receptor PPARgamma is activated in bladder cancer, either directly by gene amplification or

155 f an association between selenium levels and bladder cancer (for fourth quartile vs. first quartile,

156 e data showed a clear separation between the bladder cancer group and the control group from the disc

157 The International Bladder Cancer Group has developed formal recommendation

158 ysis of the CCNE1 region using data from two bladder cancer GWAS (5,942 cases and 10,857 controls).

159 Smoking, a well-established risk factor for bladder cancer, has been associated with lower selenium

160 d trials exploring adjuvant chemotherapy for bladder cancer have been underpowered and/or terminated

161 lomethanes (THM) with pregnancy disorders or bladder cancer have not accounted for specific household

162 m growth factor mediators of this pathway in bladder cancer have not been well delineated.

163 A genome-wide association study (GWAS) of bladder cancer identified a genetic marker rs8102137 wit

164 cystoscopy to improve clinical diagnosis of bladder cancer in clinics and at point-of-care (POC) set

165 In a case-control study of bladder cancer in Egypt, we examined the relationship be

166 o DBPs was associated with increased risk of bladder cancer in humans.

167 nidase, an enzyme previously associated with bladder cancer in humans.

168 nfection byproducts has been associated with bladder cancer in multiple studies.

169 Crude incidences of bladder cancer in pioglitazone users and nonusers were 8

170 elenium has been linked to a reduced risk of bladder cancer in some studies.

171 ells to the development of luminal and basal bladder cancers in animal models.

172 In contrast, for invasive bladder cancer, incidence was more strongly elevated in

173 Bladder cancer incurs a higher lifetime treatment cost t

174 ry epithelial cells and increases breast and bladder cancer invasion and metastasis.

175 Bladder cancer is a common and deadly malignancy but its

176 Bladder cancer is a common disease whose natural history

177 Bladder cancer is a complex disease associated with high

178 Bladder cancer is a highly prevalent human disease in wh

179 Plasmacytoid bladder cancer is an aggressive histologic variant with

180 y care for patients with MIBC and metastatic bladder cancer is critical.

181 e current gold standard for the diagnosis of bladder cancer is cystoscopy, which is invasive and pain

182 sis of gene expression data of patients with bladder cancer is finally proposed.

183 Bladder cancer is the fifth most common in incidence and

184 Bladder cancer is the health end point used by the Unite

185 High-grade T1 (HGT1) bladder cancer is the highest risk subtype of non-muscle

186 In human bladder cancer, luminal and basal forms have dissimilar

187 ntly by increased rates of lung, kidney, and bladder cancer, lymphoma, leukemia, and unspecified meta

188 generative processes, and human schistosomal bladder cancers may shed new light on the complex biolog

189 RhoGDI2 specifically suppresses bladder cancer metastasis but not primary tumor growth,

190 pathway and potential therapeutic target in bladder cancer metastasis.

191 uman subjects, and human cell line models of bladder cancer metastasis.

192 Muscle-invasive bladder cancer (MIBC) generally responds poorly to treat

193 Muscle Invasive Bladder Cancer (MIBC) has a poor prognosis.

194 e microenvironment of cancer.Muscle-invasive bladder cancer (MIBC) is a potentially lethal disease.

195 Muscle-invasive bladder cancer (MIBC) is an aggressive disease with limi

196 as the standard of care for muscle-invasive bladder cancer (MIBC), radiotherapy-based, bladder-spari

197 d-modality therapy (CMT) for muscle-invasive bladder cancer (MIBC), reserving cystectomy for salvage

198 advance has been achieved in muscle-invasive bladder cancer (MIBC).

199 Muscle-invasive bladder cancers (MIBCs) are biologically heterogeneous a

200 Restoration of STAG2 expression in a mutated bladder cancer model alleviates the dependency on STAG1.

201 he incidence of MIBCs in a murine orthotopic bladder cancer model and decreased the expression of ins

202 ve efficacy of cisplatin NP in a stroma-rich bladder cancer model.

203 Discrete bladder cancer molecular subtypes exhibit differential c

204 For muscle-invasive bladder cancer, multimodal treatment involving radical c

205 Comparison with muscle-invasive bladder cancer mutation profiles revealed lower overall

206 patients with high-risk non-muscle-invasive bladder cancer (NMIBC) are either refractory to bacillus

207 on of fibulin-3 in T2 vs non-muscle-invasive bladder cancer (NMIBC) by quantitative reverse transcrip

208 Non-muscle-invasive bladder cancer (NMIBC) is a highly recurrent tumor despi

209 ression in patients with non-muscle-invasive bladder cancer (NMIBC).

210 Calmette-Guerin (BCG) for nonmuscle invasive bladder cancer (NMIBC).

211 leukaemia, genitourinary cancers other than bladder cancer, non-Hodgkin lymphoma, lung cancer, leuka

212 First to fourth recurrences of bladder cancer occurred in 313, 174, 103, and 66 patient

213 Bladder cancer, one of the most frequently occurring hum

214 urvival of mice inoculated with either human bladder cancer or fibrosarcoma cells.

215 y have potential as biomarkers of aggressive bladder cancer or therapeutic targets.

216 some of our findings present rare events in bladder cancer, our study suggests that comprehensively

217 an inverse association between selenium and bladder cancer overall, our results, combined with an in

218 ection criteria for early cystectomy in HGT1 bladder cancer, particularly for patients with deep lami

219 two mesenchymal cell lines from ascites of a bladder cancer patient (i.e. cells already migrated outs

220 of urinary EVs was significantly elevated in bladder cancer patients (n = 16) compared to healthy con

221 itivity of 81.3% at a specificity of 90% (16 bladder cancer patients and 8 healthy controls).

222 g significant metabolites that differentiate bladder cancer patients and their controls in a metabolo

223 We included cTanyN1-3M0 bladder cancer patients from the National Cancer Data Ba

224 ation from the pre- and post-treatment CT of bladder cancer patients has the potential to assist in a

225 ting two types of miRNAs in urine samples of bladder cancer patients in a single reaction, with a det

226 cancer by analyzing urine glycoproteins from bladder cancer patients or matched healthy individuals.

227 standard clinical and pathologic features in bladder cancer patients.

228 ladder tumor samples from 30 muscle-invasive bladder cancer patients.

229 our findings support the utility of BTCs and bladder cancer PDX models in the discovery of novel mole

230 emotherapy in patients with locally advanced bladder cancer postcystectomy who did not receive chemot

231 r cancer tissues and used publicly available bladder cancer profiling studies to prioritize different

232 l co-activator that has been associated with bladder cancer progression and cisplatin resistance in o

233 bladder cancer to identify key regulators of bladder cancer progression and/or invasion.

234 owever, the regulatory roles of macroH2A1 on bladder cancer progression have not been fully elucidate

235 oles and mechanisms of TGF-beta signaling in bladder cancer progression in vivo for the first time.

236 ermine the function of TGF-beta signaling in bladder cancer progression, we conditionally knocked out

237 of Urology guideline on MIBC and metastatic bladder cancer, published online in March 2015, are clea

238 smoking independently increased the risk of bladder cancer, relative risk, 11.7 (P = 0.0013) and 5.6

239 Recent advances in bladder cancer research have enhanced our understanding

240 utations in NOTCH1 and NOTCH2 found in human bladder cancers result in loss of function.

241 use of pioglitazone was not associated with bladder cancer risk (adjusted hazard ratio [HR], 1.06; 9

242 estimate potential increased excess lifetime bladder cancer risk as a function of increased source wa

243 In combination with established bladder cancer risk factors and other somatic and germli

244 We estimate bladder cancer risk from potential increased bromide lev

245 1) with rs11543198, was also associated with bladder cancer risk in Europeans (P = 0.045 for an addit

246 of between 10(-3) and 10(-4) excess lifetime bladder cancer risk in populations served by roughly 90%

247 and nitrite from drinking water and diet and bladder cancer risk in women.

248 variants could be useful for inclusion into bladder cancer risk prediction models.

249 However, their relationship to bladder cancer risk remains to be elucidated.

250 as identified new susceptibility alleles for bladder cancer risk that require fine-mapping and labora

251 SNP rs11543198 was associated with bladder cancer risk with odds ratio (OR) of 1.41 and P-v

252 SNP rs1014971 was associated with bladder cancer risk, increased APOBEC3B expression, and

253 independent genomic regions associated with bladder cancer risk.

254 P) occurrence metric for informing potential bladder cancer risk.

255 with r(2) >/= 0.7) associated with increased bladder cancer risk.

256 ependent susceptibility loci associated with bladder cancer risk.

257 ymphocytes was significantly associated with bladder cancer risk.

258 ed frequency of CAs in blood lymphocytes and bladder cancer risk.

259 Evaluation of human bladder cancer samples revealed that tumors with low lev

260 In clinical bladder cancer specimens, expression of GON4L, YY1, and

261 transcript and ZEB2 protein levels in human bladder cancer specimens.

262 f gene lists in different domains including: bladder cancer staging, tumour site of origin and mislab

263 sted for antiproliferative activity on human bladder cancer T24 cells.

264 sitivity was higher for initial diagnosis of bladder cancer than for diagnosis of recurrence.

265 years have shed light on genetic subtypes of bladder cancer that might differ from one another in res

266 wever, for some malignancies such as urinary bladder cancer, the ability to accurately assess local e

267 For non-muscle-invasive bladder cancer, the mainstay of treatment is complete re

268 In human bladder cancers, the highest levels of phosphorylated SM

269 e understanding of HSP90 inhibition-mediated bladder cancer therapeutics.

270 of the BASE47 subtypes for standard of care bladder cancer therapies, as well as novel subtype-speci

271 tle is known about HSP90 inhibition-mediated bladder cancer therapy.

272 We performed RNA-Seq on T1 and T2 bladder cancer tissues and used publicly available bladd

273 es differentially expressed between T1 vs T2 bladder cancer to identify key regulators of bladder can

274 o curtail the M-MDSC compartment and improve bladder cancer treatment.

275 e-wide association studies (GWAS) of urinary bladder cancer (UBC) have yielded common variants at 12

276 Urinary bladder cancer (UBC) patients at muscle invasive stage h

277 ncer (BC), prostate cancer (PC), and urinary bladder cancer (UBC), and is therefore an important targ

278 (HER) 1/HER2-positive metastatic urothelial bladder cancer (UBC).

279 ematuria, anemia, dysuria, stunting, uremia, bladder cancer, urosepsis, and human immunodeficiency vi

280 ere made of samples from a few patients with bladder cancer using the NMP22 MIP-coated ZnO nanorods e

281 2 protein), a biomarker for the diagnosis of bladder cancer, using an n-type polycrystalline silicon

282 after kidney, ureter and mixed stones while bladder cancer was increased most after bladder stones.

283 ial harm from delay of RC, especially if the bladder cancer was resistant to chemotherapy.

284 The guideline on MIBC and metastatic bladder cancer was reviewed for developmental rigor by m

285 IAL/METHODS: In this study, 26 patients with bladder cancer were included.

286 OBEC3A-APOBEC3B chimera was not important in bladder cancer, whereas it was associated with breast ca

287 ASS1 expression and effects of ASS1 loss in bladder cancer which, despite affecting >70,000 people i

288 fibulin-3 serves as a pro-invasive factor in bladder cancer, which may be mediated through modulation

289 der tumors were indistinguishable from human bladder cancers, which displayed similar gene expression

290 Patients with bladder cancer with clinical lymph node involvement (cN+

291 images might be able to distinguish between bladder cancers with and without complete chemotherapy r

292 -deficient fibroblasts was also increased in bladder cancers with TSC1/TSC2 mutations in the TCGA dat

293 highest risk subtype of non-muscle-invasive bladder cancer, with highly variable prognosis, poorly u

294 , were more likely to be diagnosed as having bladder cancer within 6 months (0.70% vs 0.38%; odds rat

295 xpected in centers providing BCG therapy for bladder cancer without adequate precautions.

296 her patients underwent BCG instillations for bladder cancer without required biological precautions.

297 that administration of chemotherapy to human bladder cancer xenografts could trigger a wound-healing

298 Different bladder cancer xenografts, however, demonstrate differen

299 urs between chemotherapy cycles, using human bladder cancer xenografts.

300 EN loss, PIK3CA, AKT1, TSC1/2) are common in bladder cancer, yet small-molecule inhibitors of these n