ライフサイエンスコーパス: bladder cancer

1 cancer detection in patients with suspected bladder cancer.

2 ratumoral heterogeneity in immune markers in bladder cancer.

3 l autoimmunity and anti-PD-L1 monotherapy in bladder cancer.

4 ure and estimated the attributable burden of bladder cancer.

5 tested for the treatment of FGFR-rearranged bladder cancer.

6 der (SCCB) is a rare and lethal phenotype of bladder cancer.

7 tte smoking contribute to the development of bladder cancer.

8 (anti-PD-L1) monotherapy to chemotherapy in bladder cancer.

9 he protocol for treating non-muscle invasive bladder cancer.

10 -1 immunotherapy occur but are infrequent in bladder cancer.

11 s a putative effector of FGFR3 signalling in bladder cancer.

12 tive T cell therapy targeting neoantigens in bladder cancer.

13 ciated with cisplatin resistance in lung and bladder cancer.

14 d as a potential therapeutic target in human bladder cancer.

15 cer (MIBC) represents 25% of newly diagnosed bladder cancer.

16 s commonly up-regulated in cancer, including bladder cancer.

17 ts with BCG-unresponsive non-muscle-invasive bladder cancer.

18 l evaluated in patients with muscle invasive bladder cancer.

19 ts with BCG-unresponsive non-muscle-invasive bladder cancer.

20 ple-negative breast cancer and one (<1%) had bladder cancer.

21 as non-small cell lung carcinoma (NSCLC) and bladder cancer.

22 ariety of malignancies, including metastatic bladder cancer.

23 tro, and Pparg mutations are associated with bladder cancer.

24 nt, and ultimately outcome for patients with bladder cancer.

25 bladder-sparing treatment of muscle-invasive bladder cancer.

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

27 in consultation for management of recurrent bladder cancer.

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

29 an association between swimming pool use and bladder cancer.

30 eatment of advanced human cancers, including bladder cancer.

31 er discovery or chemoradiation strategies in bladder cancer.

32 e kinase (RTK) signaling frequently occur in bladder cancer.

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

34 ing has identified the genes most mutated in bladder cancer.

35 iated with adverse reproductive outcomes and bladder cancer.

36 apy for BCG-unresponsive non-muscle-invasive bladder cancer.

37 a specific inhibitor of LAT1, was studied in bladder cancer.

38 ssion profile and functional role of LAT1 in bladder cancer.

39 as in the peripheral blood of patients with bladder cancer.

40 nce of carcinoma in situ, and prior low-risk bladder cancer.

41 ay provide potential therapeutic targets for bladder cancer.

42 egarding the classification and treatment of bladder cancer.

43 ced melanoma, non-small cell lung cancer, or bladder cancer.

44 focusing on 95 genes known to be mutated in bladder cancer.

45 fectors YAP and TAZ is frequently altered in bladder cancer.

46 ve therapy for high-risk non-muscle-invasive bladder cancer.

47 orrelated with the progression status of the bladder cancers.

48 ession of TP63 and highly expressed in basal bladder cancers.

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

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

51 cascade components that are up-regulated in bladder cancers.

52 infections, is associated with prostate and bladder cancers.

53 the precursor lesion of most muscle-invasive bladder cancers.

54 colon cancer, 0.98 (95% CI: 0.49, 1.97) for bladder cancer, 1.02 (95% CI: 0.59, 1.78) for lung cance

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

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

57 ses correlating to the basal centroid of the bladder cancer analysis of subtypes by gene expression 4

58 thelial carcinoma is the most common type of bladder cancer and accounts for 90% of bladder cancer ca

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

60 r, with BCG-unresponsive non-muscle-invasive bladder cancer and an Eastern Cooperative Oncology Group

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

62 post treatment surveillance in patients with bladder cancer and cancer detection in patients with sus

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

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

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

66 B), and is also used as an immunotherapy for bladder cancer and other malignancies due to its immunos

67 as possible increased risk for death due to bladder cancer and pneumonitis.

68 analyses of mouse and human model systems of bladder cancer and show that tumor cells with multiple l

69 s have been shown to cure some patients with bladder cancer and significantly decrease adverse events

70 ion on first-line immunotherapy for advanced bladder cancer and subsequent changes in practice.

71 ated TIL cultures from patients with primary bladder cancer and tested their ability to recognize tum

72 mechanisms of FOXA1 and PTEN inactivation in bladder cancer and their contribution to tumor heterogen

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

74 tion of BCG-unresponsive non-muscle-invasive bladder cancer and were therefore excluded from efficacy

75 Understanding the molecular features of T1 bladder cancers and how they respond to BCG therapy coul

76 4) gene loci in liver cancer, HPV and BKV in bladder cancer, and EBV in non-Hodgkin's lymphoma.

77 tiation between metastatic and nonmetastatic bladder cancer, and nonmetastatic cancer from healthy in

78 l cancer subtypes, as well as non-urothelial bladder cancers, and discuss how the integration of geno

79 Breast cancers, bladder cancers, and uterine cancers have spatial patter

80 ations in clinical staging, patients with T1 bladder cancer are at risk of both undertreatment with p

81 Advanced prostate and bladder cancer are two outstanding unmet medical needs f

82 t the factor(s) regulating its expression in bladder cancer are unknown.

83 y of the genetic features of muscle-invasive bladder cancers, are classified as non-muscle-invasive o

84 cade and (2) establish the utility of canine bladder cancer as a naturally-occurring model for human

85 -fixed paraffin-embedded (FFPE) tissue using bladder cancer as an exemplar; and (2) examine the influ

86 e in order to estimate odds ratios (ORs) for bladder cancer associated with the mean THM level in eac

87 s that are expressed differentially in human bladder cancer-associated blood vessels to find novel bi

88 ensing of apolipoprotein A1 (ApoA1) in early bladder cancer (BC) diagnosis and prognosis monitoring.

89 Bladder cancer (BC) is heterogeneous and expresses vario

90 Because the evidence of association with bladder cancer (BC) is limited, we aimed to assess assoc

91 Because bladder cancer (BC) is one of the most common malignant

92 Invasive bladder cancer (BC) is one of the most lethal malignant

93 suggest that patients with a basal/stem-like bladder cancer (BC) subtype tend to have metastatic dise

94 lf a million US residents are suffering with bladder cancer (BC), which costs a total $4 billion in t

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

96 protein, is overexpressed in people who have bladder cancer (BC).

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

98 rbohydrate-binding proteins overexpressed in bladder cancer (BCa) cells.

99 nuclear androgen receptor (nAR) to increase bladder cancer (BCa) progression, the impact of androgen

100 med limited drug testing on organoids in the bladder cancer biobank.

101 Advanced Bladder Cancer (BLCA) remains a clinical challenge that

102 C1) activated kinase 4 (PAK4) in a subset of Bladder cancer (BLCA).

103 s of cisplatin and gemcitabine on basal-like bladder cancer both in vivo and in vitro.

104 drives tumor formation and invasion in human bladder cancers but the factor(s) regulating its express

105 been the mainstay of treatment for advanced bladder cancer, but high-quality evidence is lacking to

106 ction for average residential THM levels and bladder cancer by pooling data from studies included in

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

108 mic profiling studies have demonstrated that bladder cancer can be divided into two molecular subtype

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

110 % CI: 1,522, 4,060; 43%) annual attributable bladder cancer cases could potentially be avoided.

111 e fraction (PAF), and number of attributable bladder cancer cases in different scenarios using incide

112 pe of bladder cancer and accounts for 90% of bladder cancer cases in the USA and Europe.

113 accounting for 6,561 (95% CI: 3,389, 9,537) bladder cancer cases per year.

114 rotein degradation by miR-934 promotes human bladder cancer cell growth.

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

116 Silencing or inhibition of mutant FGFR3 in bladder cancer cell lines is associated with decreased m

117 tant FGFR3, as its knockdown in FGFR3-mutant bladder cancer cell lines is associated with reduced pro

118 tients and analysis of distinct melanoma and bladder cancer cell lines suggested differences in cance

119 addition, FOXA1 is hypermethylated in basal bladder cancer cell lines, and this is reversed by treat

120 PolH in various cisplatin-resistant lung and bladder cancer cell lines.

121 studies in patients with advanced cancer, in bladder cancer cell lines.

122 R complex 2 (mTORC2) is a major regulator of bladder cancer cell migration and invasion, but the mech

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

124 ch achieves highly specific capture rates of bladder cancer cells based on their Epithelial Cell Adhe

125 new screening membrane receptor platform for bladder cancer cells by integrating surface-enhanced Ram

126 gger AMPK-dependent autophagic cell death in bladder cancer cells by PI3K/AKT/HIF-1alpha-mediated gly

127 K2 significantly promoted the glycolysis in bladder cancer cells by upregulating glucose consumption

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

129 The pronounced glycocalyx of bladder cancer cells enhanced the internalisation of nan

130 oundly abrogated AMPK activation and rescued bladder cancer cells from Vitamin K2-triggered autophagi

131 promotes the apoptosis of T24 and 5637 human bladder cancer cells in a concentration-dependent manner

132 ar gammadelta T-cell-mediated eradication of bladder cancer cells in vitro.

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

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

135 hole cell immunocapture technology to detect bladder cancer cells shed in patient urine ex vivo.

136 In the present study, we found CNF1 induced bladder cancer cells to secrete vascular endothelial gro

137 Finally, we found that 9-ING-41 sensitized bladder cancer cells to the cytotoxic effects of human i

138 LAT1 expression in bladder cancer cells was higher than that in normal cell

139 In breast and bladder cancer cells with high p27pT157pT198 or expressi

140 as well as whole transcriptome sequencing of bladder cancer cells {plus minus} tet-on ZFP36L1 was per

141 nses to targets were obtained by grade-I RT4 bladder cancer cells, NIH/3T3 fibroblast cells, and SV-H

142 Using bladder cancer cells, we confirmed the role of PAK4 in B

143 ine or cisplatin when used in combination in bladder cancer cells.

144 3K/AKT and HIF-1alpha-mediated glycolysis in bladder cancer cells.

145 rogression of chemical-transformed cells and bladder cancer cells.

146 anin B on the proliferation and apoptosis of bladder cancer cells.

147 ium and an efficient culture system of human bladder cancer cells.

148 ell cycle arrest, autophagy and apoptosis in bladder cancer cells.

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

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

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

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

153 tive and migratory and invasive abilities in bladder cancer cells.

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

155 e and provides an important resource for the bladder cancer community.

156 Adjusted ORs for bladder cancer comparing participants with exposure abov

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

158 scriptomic and proteomic characterization of bladder cancer could guide future therapies.

159 development and progression of prostate and bladder cancer could yield key insights to inform the cl

160 ) are typically extrapolated from studies of bladder cancer despite their distinct clinical and molec

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

162 o found positively correlated with the human bladder cancer development.

163 ltiple microbiopsies from five patients with bladder cancer enabled comparisons with cancer-free indi

164 inal cells in mice results in development of bladder cancer exhibiting squamous features as well as e

165 d insight into the mechanisms underlying the bladder cancer field effect and tumor recurrence.

166 Death resulting from bladder cancer (for >2.56 ppm vs. unexposed, lagged 10-y

167 ereas mutations were absent in several major bladder cancer genes.

168 ing of the molecular biology and genetics of bladder cancer has evolved the way localized and advance

169 our understanding of the cellular aspects of bladder cancer has grown.

170 Molecular subtyping of bladder cancer has identified an aggressive basal subtyp

171 Sequencing of bladder cancer has revealed that loss-of-function mutati

172 The field of research in bladder cancer has seen significant advances in recent y

173 Yet, patients with T1 bladder cancer have an overall mortality of 33% and a ca

174 High-grade nonmuscle invasive bladder cancer (HRNMIBC) is a heterogeneous disease.

175 nate (HAL) during transurethral resection of bladder cancer improves detection of non-muscle-invasive

176 for the inclusion of patients with advanced bladder cancer in clinical studies of 9-ING-41.

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

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

179 n order to facilitate molecular subtyping of bladder cancer in primary care centers, we analyzed the

180 tool for assessment of molecular subtypes of bladder cancer in routine clinical practice.

181 howing promising results in the treatment of bladder cancer, including infigratinib and pemigatinib,

182 Bladder cancer incurs a higher lifetime treatment cost t

183 The invasion of bladder cancer into the sub-urothelial muscle and vascul

184 ingle gene expression signatures to classify bladder cancers into distinct subtypes.

185 Stage T1 bladder cancers invade the lamina propria of the bladder

186 investigating intracellular heterogeneity of bladder cancer invasion and analyzing patient derived sa

187 mbly approach for recapitulating features of bladder cancer invasion in 3D microenvironments and prob

188 pitulate the pathobiological events of human bladder cancer invasion in mice.

189 The involvement of DLL4 expressing cells in bladder cancer invasion was also observed in patient sam

190 provide a physiological context for studying bladder cancer invasion within 3D microenvironments and

191 role of NOTCH1-DLL4 signaling in collective bladder cancer invasion.

192 Intratumoral heterogeneity in bladder cancer is a barrier to accurate molecular sub-cl

193 Bladder cancer is a common malignancy in women and is th

194 Bladder cancer is a common malignancy that has a relativ

195 Bladder cancer is a heterogeneous group of tumours with

196 iability in the outcomes of patients with T1 bladder cancer is a result of both tumour heterogeneity

197 Bladder cancer is an increasingly common malignancy, and

198 ingly common malignancy, and muscle invasive bladder cancer is associated with particularly high rate

199 Bladder cancer is common and has one of the highest recu

200 However, precise grading in bladder cancer is critical for therapeutic decision maki

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

202 y monitoring, and early relapse detection in bladder cancer is feasible and provides a basis for clin

203 nificant therapeutic impact on patients with bladder cancer is found in the use of immune checkpoint

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

205 llus Calmette-Guerin (BCG) immunotherapy for bladder cancer is the only bacterial cancer therapy appr

206 Bladder cancer is the tenth most common cancer type worl

207 1) is a key UPEC toxin; however, its role in bladder cancer is unknown.

208 ffects in patients with lung adenocarcinoma, bladder cancer, low-grade glioma, and thyroid carcinoma.

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

210 irmation but suggest that management of HGT1 bladder cancer may be improved via molecular characteriz

211 Muscle-invasive bladder cancer (MIBC) is a heterogeneous disease that of

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

213 Muscle-invasive bladder cancer (MIBC) represents 25% of newly diagnosed

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

215 In muscle-invasive bladder cancer (MIBC), the evidence shows comparable cli

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

217 nt predictors of survival in muscle-invasive bladder cancer (MIBC).

218 ), leading to subsequent angiogenesis in the bladder cancer microenvironment.

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

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

221 le invasive (HGT1) micropapillary variant of bladder cancer (MPBC).

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

223 Common bladder cancer mutations like TP53 and FGFR3 were found

224 s received mBCG, four had nonmuscle invasive bladder cancer (NMIBC) after induction, three had NMIBC

225 er improves detection of non-muscle-invasive bladder cancer (NMIBC) and reduces recurrence rates.

226 Non-muscle-invasive bladder cancer (NMIBC) remains one of the most common ma

227 genes frequently affected in muscle-invasive bladder cancer of nonpapillary origin, focusing on poten

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

229 Human bladder cancer organoids can be derived efficiently from

230 ids to create a living biobank consisting of bladder cancer organoids derived from 53 patients.

231 These so-called bladder (cancer) organoids consist of 3D structures of e

232 Although advanced bladder cancer overall has a poor prognosis, a subset of

233 enes encoding cohesin subunits are common in bladder cancers, paediatric sarcomas, leukaemias, brain

234 The estimated bladder cancer PAF was 4.9% [95% confidence interval (CI

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

236 As (microRNA-10b, -182, -143, and -145) from bladder cancer patient plasma (50 muL/sample).

237 individuals, in metastatic and nonmetastatic bladder cancer patient plasma.

238 that METTL3 and CDCP1 are upregulated in the bladder cancer patient samples and the expression of MET

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

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

241 rovides prognostic value for muscle invasive bladder cancer patients and a better model fit than TNM

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

243 can origin, and decreased immune activity in bladder cancer patients of East Asian origin.

244 edicts a clinical response in 244 metastatic bladder cancer patients treated with anti-PD-L1.

245 formed multi-omic profiling of the kinome in bladder cancer patients with the goal of identify therap

246 iagnostic tool, we analyzed the plasma of 20-bladder cancer patients without any sample processing st

247 ated with poor survival in liver, colon, and bladder cancer patients.

248 whole slide images from 100 muscle invasive bladder cancer patients.

249 y in cell lines and primary tumor cells from bladder cancer patients.

250 t SCCB shares a urothelial origin with other bladder cancer phenotypes by showing that urothelial cel

251 lecular similarities and differences between bladder cancer phenotypes.

252 The morphologic and molecular diversity of bladder cancer poses significant challenges in elucidati

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

254 Bladder cancer prognosis is closely linked to the underl

255 mechanism through which UPEC contributes to bladder cancer progression, and may provide potential th

256 lectively, LAT1 significantly contributed to bladder cancer progression.

257 lidated METTL3 as a tumor suppressor gene in bladder cancer, providing support to the important role

258 e most suitable endogenous control genes for bladder cancer qPCR.

259 Bladder cancer ranges from unaggressive and usually noni

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

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

262 been consistently associated with increased bladder cancer risk.

263 rization effect has been proposed to explain bladder cancer's multifocal and recurrent nature, yet th

264 eage tracing revealed that the stemness of a bladder cancer stem cell population was inhibited by dec

265 otherapy have led to the reclassification of bladder cancer subgroups and rigorous efforts to define

266 anoid lines contained both basal and luminal bladder cancer subtypes based on immunohistochemistry an

267 dition, given the molecular heterogeneity of bladder cancer, targeting more than one surface receptor

268 still could lead to a considerable burden of bladder cancer that could potentially be avoided by opti

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

270 ciations involve cyclin-dependent kinases in bladder cancer, the MAPK signaling pathway in lung cance

271 termediate and high-risk non-muscle-invasive bladder cancer, the therapeutic options for muscle-invas

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

273 analysis of histone modifications in primary bladder cancer tissue and provides an important resource

274 as contributors to hyaluronan degradation in bladder cancer tissue, leading to accumulation of inflam

275 anced breakdown of extracellular HA in human bladder cancer tissue, leading to the accumulation of sm

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

277 ity has never been systematically studied in bladder cancer treatment.

278 romising therapeutic approach for basal-like bladder cancer treatment.

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

280 may represent a novel therapeutic option in bladder cancer treatment.

281 tify a novel combination strategy for canine bladder cancer treatment: targeting the ErbB/MAPK signal

282 expression signature was identified between bladder cancer tumor blood vasculature with tumor blood

283 ions of signature luminal and basal genes in bladder cancer tumor samples from publicly available and

284 nt transformation of uroepithelial cells and bladder cancer tumorigenesis in vitro and in vivo.

285 Herein, an exemplary potential biomarker in bladder cancer was identified by the novel approach of F

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

287 Patients with cT2-4a muscle-invasive bladder cancer were randomly assigned to FCT or GD.

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

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

290 ests that neoantigen-reactive TILs reside in bladder cancer, which may help explain the effectiveness

291 in family have been reported in prostate and bladder cancers, which, together with the aberrant glyco

292 e which identified the molecular subtypes of bladder cancer with 80-94% sensitivity and 83-93% specif

293 highest risk subtype of non-muscle-invasive bladder cancer with unpredictable outcome and poorly und

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

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

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

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

298 nt of both Tsc2(+/) (-) mice and a TSC1-null bladder cancer xenograft model with a CDK7 inhibitor sho

299 Different bladder cancer xenografts, however, demonstrate differen

300 GF expression, and angiogenesis in the human bladder cancer xenografts.