ライフサイエンスコーパス: urothelial

1 y was to investigate the effect of ageing on urothelial-afferent signalling in the mouse bladder.

2 e observed in patients with glioblastoma and urothelial and endometrial cancer (all with FGFR2 or FGF

3 ants clinical investigation in ASS1-negative urothelial and related cancers, using FLT-PET as an earl

4 ts, with concomitant increased activation of urothelial and stromal NF-kappaB and AP1 in vivo and in

5 ncer types (gastrointestinal, breast, kidney/urothelial, and hematologic malignancies).

6 measured the stiffness of the intact, living urothelial apical membrane and found it to be highly def

7 However, the role of urothelial AR (Uro-AR) in BCa development remains unclea

8 ents of the bladder (neural, contractile and urothelial) are affected by ageing.

9 Bladder afferent nerve hyperexcitability and urothelial ATP release with CYP-induced cystitis is decr

10 ferent nerve discharge and the mechanisms of urothelial ATP release with distention.

11 rexcitability with a concomitant decrease in urothelial ATP release.

12 findings support the model that a defective urothelial barrier allows urine to induce a fibrotic wou

13 al cells undergo cell death by E17.5 and the urothelial barrier becomes leaky to luminal fluid.

14 compromised development and regeneration of urothelial barrier function.

15 lead to treatments that prevent loss of the urothelial barrier, a major cause of voiding dysfunction

16 detrimental to the establishment of a tight urothelial barrier, leading to chronic pain.

17 e administration decreased the expression of urothelial barrier-associated protein, altered HA produc

18 onditional-knockout (beta1-cKO) mice lacking urothelial beta1-integrin exhibited down-regulation and

19 jor advances for the treatment of metastatic urothelial bladder cancer (UBC) in the last 30 years.

20 or receptor (HER) 1/HER2-positive metastatic urothelial bladder cancer (UBC).

21 ogen regulated, providing the foundation for urothelial bladder cancer therapy with antiandrogens.

22 as ultimately diagnosed with muscle-invasive urothelial bladder cancer.

23 nscriptional analysis of non-muscle invasive urothelial bladder cancer.

24 ith pegfilgrastim support in muscle-invasive urothelial cancer (MIUC).

25 cancer (duration, 4 months), a patient with urothelial cancer (ongoing at >/= 19 months), and a pati

26 a standard option for patients with advanced urothelial cancer (UC) who are ineligible for cisplatin,

27 igh frequency in multiple cancers, including urothelial cancer (UC), but their effect on telomerase f

28 Current urinary diagnostic tests for urothelial cancer are expensive and have limited sensiti

29 We also observed an increased risk of urothelial cancer at eGFR<30 but no significant associat

30 th an independently higher risk of renal and urothelial cancer but not other cancer types.

31 More than half of all patients with advanced urothelial cancer cannot receive standard, first-line ci

32 ancer-associated TERT promoter mutation in a urothelial cancer cell line results in decreased telomer

33 ection of urothelial cells, where high-grade urothelial cancer cells are characterized by a large nuc

34 plications of ASS1 loss were investigated in urothelial cancer cells.

35 isclosed residual high-grade muscle-invasive urothelial cancer extending to the perivesical fat and i

36 igand 1 [PD-L1]) as treatment for metastatic urothelial cancer in cisplatin-ineligible patients.

37 A 70-year-old man with urothelial cancer of the bladder (UBC) metastatic to the

38 had a considerably higher risk of developing urothelial cancer than MLH1 or MSH6 carriers.

39 cisplatin-ineligible patients with advanced urothelial cancer who had not been previously treated wi

40 patients with locally advanced or metastatic urothelial cancer who were cisplatin ineligible.

41 xamine the mutational processes operating in urothelial cancer, a tumor type in which the core NER ge

42 PD-1 and its ligands are expressed in urothelial cancer, and findings have shown that inhibiti

43 immunohistochemistry) TNBC, gastric cancer, urothelial cancer, and head and neck cancer.

44 a history of kidney cancer, prostate cancer, urothelial cancer, and skin squamous cell carcinoma.

45 a high long-term risk for renal failure and urothelial cancer, and the potential worldwide populatio

46 diagnosis of locally advanced or metastatic urothelial cancer, including cancers of the renal pelvis

47 bility in cisplatin-ineligible patients with urothelial cancer, most of whom were elderly, had poor p

48 acceptable safety in patients with advanced urothelial cancer, supporting ongoing phase 2 and 3 stud

49 In advanced urothelial cancer, treatment with dose-dense methotrexat

50 its therapeutic use in untreated metastatic urothelial cancer.

51 c evidence of tobacco-related mutagenesis in urothelial cancer.

52 favor of high-dose-intensity chemotherapy in urothelial cancer.

53 n and malaise after resection of a papillary urothelial cancer.

54 in Balkan endemic nephropathy and associated urothelial cancer.

55 ally advanced and unresectable or metastatic urothelial cancer.

56 major improvements in survival of incurable urothelial cancer.

57 salvage chemotherapy is modest in metastatic urothelial cancer.

58 1-amplified sqNSCLC and FGFR3-mutant bladder/urothelial cancer.

59 patients with locally advanced or metastatic urothelial cancer.

60 its therapeutic use in untreated metastatic urothelial cancer.

61 istent with locally recurrent and metastatic urothelial cancer.

62 sions regarding the activity of pazopanib in urothelial cancers after failure of platinum-based chemo

63 Urothelial cancers are amongst the 10 most common types

64 N had borderline increased incidence for all urothelial cancers combined (renal pelvis, ureter, and b

65 phadenectomy data for kidney and upper tract urothelial cancers remain muddled as routine lymphadenec

66 Specifically, the risk of lung and urothelial cancers was elevated, which was evident regar

67 al benefit (DCB) in patients with metastatic urothelial cancers, including complete remissions in pat

68 ns were recently discovered in AA-associated urothelial cancers.

69 activity of paclitaxel in previously treated urothelial cancers.

70 1-amplified sqNSCLC and FGFR3-mutant bladder/urothelial cancers.

71 n paclitaxel in the second-line treatment of urothelial cancers.

72 ent of Aristolochia herbs and a potent human urothelial carcinogen.

73 sults support an association between BKV and urothelial carcinogenesis among kidney transplant recipi

74 64, 95% confidence interval: 2.92, 7.38) and urothelial carcinoma (hazard ratio = 2.02, 95% confidenc

75 eted delivery of cytotoxic drugs in invasive urothelial carcinoma (iUC), for which improved therapy i

76 Metastatic urothelial carcinoma (mUC) has a very high mutational ra

77 the BK virus (BKV) in the carcinogenesis of urothelial carcinoma (UC) after renal transplantation ar

78 variation in the ERBB family are frequent in urothelial carcinoma (UC) and may represent viable thera

79 enal cell carcinoma (RCC) and 3-fold risk of urothelial carcinoma (UC) compared with the general popu

80 fect of pre-operative renal insufficiency on urothelial carcinoma (UC) prognosis has been investigate

81 tivating mutations of PIK3CA are frequent in urothelial carcinoma (UC), no information is available o

82 treatment options for progressive metastatic urothelial carcinoma (UC).

83 suggested an overlap of CDC with upper tract urothelial carcinoma (UTUC), making the pathological dia

84 cal nephroureterectomy (RNU) for upper tract urothelial carcinoma (UTUC).

85 excision (RNU) for patients with upper tract urothelial carcinoma (UTUC).

86 patients with locally advanced or metastatic urothelial carcinoma after progression with platinum-bas

87 is clonally enriched in chemotherapy-treated urothelial carcinoma and continues to shape the evolutio

88 or therapeutic use of avelumab in metastatic urothelial carcinoma and it has received accelerated US

89 as a tumor-suppressor gene in urinary tract urothelial carcinoma and may be an innovative co-targeti

90 e from chemotherapy directs the evolution of urothelial carcinoma and shapes its clonal architecture

91 However, greater understanding of urothelial carcinoma and solid tumor biology has resulte

92 Despite a high prevalence of urothelial carcinoma and the risk of bladder carcinoma,

93 The majority of targeted agents studied in urothelial carcinoma are in the second-line setting; new

94 transformed human urothelial cells and many urothelial carcinoma cell lines exhibit constitutive HH

95 the difference in intrinsic HH dependence of urothelial carcinoma cell lines, a gene expression signa

96 elial cells and from low-grade to high-grade urothelial carcinoma cell lines, whereas alternatively s

97 issues and promotes motility and invasion of urothelial carcinoma cells.

98 es that have been reported or are in ongoing urothelial carcinoma clinical trials, and highlight mole

99 model for investigating sexual dimorphism in urothelial carcinoma development, and implicated synergy

100 secutive adults with metastatic, progressive urothelial carcinoma enrolled in a National Cancer Insti

101 Chemotherapy-resistant urothelial carcinoma has no uniformly curative therapy.

102 Patients with metastatic urothelial carcinoma have a dismal prognosis and few tre

103 Patients with metastatic urothelial carcinoma have few treatment options after fa

104 ureterectomy, disclosing residual high-grade urothelial carcinoma infiltrating the full thickness of

105 sy identified transitional cell carcinoma or urothelial carcinoma invading the muscularis propria of

106 Upper urinary tract urothelial carcinoma is a relatively uncommon disease an

107 in-ineligible locally advanced or metastatic urothelial carcinoma is associated with short response d

108 d several insights: (i) chemotherapy-treated urothelial carcinoma is characterized by intra-patient m

109 helial carcinoma; (iii) chemotherapy-treated urothelial carcinoma is enriched with clonal mutations i

110 understanding of the biology and genetics of urothelial carcinoma is helping to identify and define t

111 Development of targeted therapies for urothelial carcinoma is still in early stages, consequen

112 Urothelial carcinoma is the most common type of bladder

113 3) occur in up to 80% of low-grade papillary urothelial carcinoma of the bladder (LGP-UCB) suggesting

114 p of stagnant mortality rates for metastatic urothelial carcinoma of the bladder (mUCB) at presentati

115 cal management of human cancer, including in urothelial carcinoma of the bladder (UCB).

116 Patients with muscle-invasive urothelial carcinoma of the bladder have poor survival a

117 expression to be associated with aggressive urothelial carcinoma of the bladder, as well as increase

118 Eligible patients had histologically proven urothelial carcinoma of the bladder, pT3-pT4 disease or

119 cystectomy in patients with pT3-pT4 or N+ M0 urothelial carcinoma of the bladder.

120 both nonmuscle-invasive and muscle-invasive urothelial carcinoma of the bladder.

121 we enrolled patients (age >/=18 years) with urothelial carcinoma of the renal pelvis, ureter, bladde

122 patients with platinum-refractory metastatic urothelial carcinoma overexpressing PD-L1 (IC2/3).

123 multicenter, expansion cohort, patients with urothelial carcinoma progressing after platinum-based ch

124 patients with locally advanced or metastatic urothelial carcinoma receiving second-line treatment and

125 es of combined hazard ratio (HR) for bladder urothelial carcinoma recurrence, cancer-specific surviva

126 ), respectively; and for upper urinary tract urothelial carcinoma recurrence, CSS and OS were 2.27 (9

127 xome sequencing and clonality analysis of 72 urothelial carcinoma samples, including 16 matched sets

128 lly confirmed locally advanced or metastatic urothelial carcinoma that had progressed after at least

129 treatments exist for patients with advanced urothelial carcinoma that has progressed after platinum-

130 noma and continues to shape the evolution of urothelial carcinoma throughout its lifetime.

131 (TCR) clonality inform clinical outcomes in urothelial carcinoma treated with atezolizumab.

132 Urothelial carcinoma was the most common malignancy afte

133 April 24, 2015, 86 patients with metastatic urothelial carcinoma were enrolled in the nivolumab mono

134 2016, 329 patients with advanced metastatic urothelial carcinoma were screened for enrolment into th

135 Patients (aged >/=18 years) with metastatic urothelial carcinoma who had progressed after platinum-b

136 rial in patients with advanced or metastatic urothelial carcinoma who progressed during or after plat

137 th inoperable locally advanced or metastatic urothelial carcinoma whose disease had progressed after

138 patients with locally advanced or metastatic urothelial carcinoma whose disease progressed after prev

139 s with metastatic or surgically unresectable urothelial carcinoma whose disease progressed or recurre

140 The incidence for bladder urothelial carcinoma, a common malignancy of the urinary

141 rs different tumor biology than that of pure urothelial carcinoma, and if this difference translates

142 xclusion criteria were obstructive uropathy, urothelial carcinoma, and metastatic cancer.

143 or surgically unresectable locally advanced urothelial carcinoma, measurable disease (according to R

144 dentified in conventional and micropapillary urothelial carcinoma, small cell, and squamous cell carc

145 In the first-line treatment of metastatic urothelial carcinoma, tubulin, cytotoxic T-lymphocyte an

146 Pathology revealed pathologic extravesical urothelial carcinoma, with disease in one of 25 lymph no

147 patients with locally advanced or metastatic urothelial carcinoma.

148 response to this class of agents in advanced urothelial carcinoma.

149 ed carcinoma-in-situ to high-grade papillary urothelial carcinoma.

150 adenectomy for patients with muscle-invasive urothelial carcinoma.

151 may inform the progression and treatment of urothelial carcinoma.

152 variably lost during progression to invasive urothelial carcinoma.

153 body, in patients with refractory metastatic urothelial carcinoma.

154 s with metastatic or surgically unresectable urothelial carcinoma.

155 losely resembled that of the human low-grade urothelial carcinoma.

156 , biopsy of which showed invasive high-grade urothelial carcinoma.

157 n patients with platinum-refractory advanced urothelial carcinoma.

158 erapeutic treatment option for patients with urothelial carcinoma.

159 h platinum-refractory advanced or metastatic urothelial carcinoma.

160 patients with locally advanced or metastatic urothelial carcinoma.

161 igation of nivolumab monotherapy in advanced urothelial carcinoma.

162 patients with locally advanced or metastatic urothelial carcinoma.

163 very early events in the natural history of urothelial carcinoma; (iii) chemotherapy-treated urothel

164 patients with platinum-refractory metastatic urothelial carcinoma; a manageable safety profile was re

165 ous cell carcinomas (SCC, OR = 4.90) than in urothelial carcinomas (UC, OR = 3.62).

166 We recently defined molecular subtypes of urothelial carcinomas according to whole genome gene exp

167 egregation, in 36% of papillary non-invasive urothelial carcinomas and 16% of invasive urothelial car

168 enhance chemotherapeutic response of bladder urothelial carcinomas by abrogating early tumour repopul

169 sue microarrays with 693 non-muscle invasive urothelial carcinomas from Danish, Swedish, and Spanish

170 microarrays (TMAs) with a total of 859 Ta/T1 urothelial carcinomas from Danish, Swedish, Spanish, and

171 mpound found in certain herbal medicines, in urothelial carcinomas of exposed populations.

172 Muscle-invasive urothelial carcinomas of the bladder (MIUCB) exhibit fre

173 ve urothelial carcinomas and 16% of invasive urothelial carcinomas of the bladder.

174 Eleven patients presented with urothelial carcinomas of the upper tract; 2 of them with

175 ic value of the protein expressions in Ta/T1 urothelial carcinomas patients.

176 ons, infections, and cancers with a focus on urothelial carcinomas, are reported.

177 he ICG pHLIP imaging agent marked high-grade urothelial carcinomas, both muscle invasive and nonmuscl

178 characterized papillary and flat noninvasive urothelial carcinomas, including 28 pTa low-grade transi

179 as, liposarcomas, hepatocellular carcinomas, urothelial carcinomas, squamous cell carcinomas of the t

180 per tract; 2 of them with additional bladder urothelial carcinomas.

181 interest in the role of Wnt/beta-catenin in urothelial carcinomas.

182 iptase (TERT) gene in 66% of muscle-invasive urothelial carcinomas.

183 atures for outcome prediction in stage Ta/T1 urothelial carcinomas.

184 nd survivin in patients with stage Ta and T1 urothelial carcinomas.

185 gement of high-risk NMI disease for standard urothelial cell carcinoma (early cystectomy vs. intraves

186 plasma carotenoids and vitamin C and risk of urothelial cell carcinoma (UCC) in a case-control study

187 Current standard of care for muscle-invasive urothelial cell carcinoma (UCC) is surgery along with pe

188 ll-characterized series of 327 patients with urothelial cell carcinoma of bladder.

189 and its metabolites were examined by primary urothelial cell culture.

190 ariectomized mice with defective superficial urothelial cell differentiation.

191 y dispensable for detrusor smooth muscle and urothelial cell fate determination, the mutants have sig

192 l voiding behaviour, sensory nerve activity, urothelial cell function, muscle contractility, transmit

193 In urothelial cell invasion assays, a speA mutant exhibited

194 ased both putrescine stimulated swarming and urothelial cell invasion in a speA mutant.

195 As urothelial cell lines with FGFR3 fusions are extremely s

196 lation of reactive oxygen species as well as urothelial cell proliferation.

197 d concentrations of As species in exfoliated urothelial cells (EUC) as an alternative to the measures

198 IK3CA mutations in immortalized normal human urothelial cells (NHUC) and mouse fibroblasts (NIH3T3).

199 of the fusions in immortalized normal human urothelial cells (NHUC) induced activation of the mitoge

200 in the binary classification of normal human urothelial cells and bladder cancer cells by reducing th

201 cute cytoplasmic biofilms within superficial urothelial cells and can persist by establishing membran

202 cultures of highly regenerative normal human urothelial cells and from low-grade to high-grade urothe

203 We show that transformed human urothelial cells and many urothelial carcinoma cell line

204 he absence of Oct4A in normal and neoplastic urothelial cells and tissues, but indicated the presence

205 Recently, the ability of UPEC to invade urothelial cells and to form intracellular bacterial com

206 mechanism of direct toxicity of ketamine to urothelial cells by activating the intrinsic apoptotic p

207 ta1-Integrin localized to basal/intermediate urothelial cells by confocal microscopy.

208 Infection of immature urothelial cells can result in the formation of persiste

209 enic mice that RTK/RAS pathway activation in urothelial cells causes hyperplasia that neither progres

210 of planktonic bacteria with cultures of shed urothelial cells concentrated in centrifuged urinary sed

211 the upregulation of which is associated with urothelial cells expressing multiple progenitor/stem cel

212 d, expressing FGFR3b-S249C in cultured human urothelial cells expressing SV40T, which functionally in

213 waaP, waaY, and rfaG attenuated adherence to urothelial cells in vitro In a murine UTI model, the Del

214 e forced expression of Oct4A in normal human urothelial cells in vitro profoundly inhibited growth an

215 Treatment of primary urothelial cells in vitro with ketamine or urine obtaine

216 ocation of the androgen receptor (AR) in the urothelial cells is a critical mechanism contributing to

217 Conditional inactivation of p53 in urothelial cells of transgenic mice expressing HRAS* res

218 on is available on their specific effects in urothelial cells or the basis for the observed mutation

219 FGFR3 mutation in human LGP-UCB, in cultured urothelial cells resulted in slightly reduced surface tr

220 ates the neoplastic transformation of normal urothelial cells to carcinoma.

221 These Sec10-knockout urothelial cells undergo cell death by E17.5 and the uro

222 n the second step, Raman spectral imaging of urothelial cells was performed.

223 of the terminally differentiated superficial urothelial cells was transcriptionally up-regulated.

224 ism; however, normal (nonimmortalized) human urothelial cells were unresponsive to NMDAR agonists or

225 matically differentiate normal and cancerous urothelial cells with 100% accuracy.

226 d confocal microscopy looking for exfoliated urothelial cells with IB.

227 on, guidance for terminal differentiation of urothelial cells, and proper investment of ureteral smoo

228 4-dependent inflammatory cell death in human urothelial cells, and we demonstrate that the response r

229 dder, namely umbrella and basal-intermediate urothelial cells, as well as the muscularis propria.

230 In urothelial cells, IL-1beta stimulation increased Cx43 ex

231 ous architectural aberrations of superficial urothelial cells, including increases in multivesicular

232 On overexpression in urothelial cells, it impairs correct tight junction form

233 d in the first step for fast preselection of urothelial cells, where high-grade urothelial cancer cel

234 on by Escherichia coli into the cytoplasm of urothelial cells, with persistence of long-term bacteria

235 3-dependent inflammatory cell death in human urothelial cells.

236 /AR signaling in carcinogenesis of the basal urothelial cells.

237 expanding and sustaining the accumulation of urothelial CSCs.

238 ted in mature bladder urothelium and primary urothelial cultures.

239 transcriptional regulator involved in human urothelial cytodifferentiation.

240 present study investigated bladder injury by urothelial defect and HA degeneration and bladder repair

241 and retinoid signaling that is essential for urothelial development and regeneration.

242 For patients with other variants of urothelial differentiation (i.e., micropapillary, sarcom

243 s with embryonic bladder mesenchyme promoted urothelial differentiation of PPARgamma2-deficient BHPrE

244 inactivation and the effect of FOXA1 loss on urothelial differentiation remain unknown.

245 The importance of ELF3 in urothelial differentiation was verified by knockdown in

246 have characteristics of different stages of urothelial differentiation, reflect the luminal and basa

247 altered HA production, and induced abnormal urothelial differentiation, which might attribute to uro

248 l expression of BMP signals, which stimulate urothelial differentiation.

249 PPARgamma is also implicated in urothelial differentiation.

250 e investigated the mechanism and dynamics of urothelial exfoliation in the early acute stages of infe

251 The mechanisms underlying urothelial formation and maintenance are largely unknown

252 data suggest that ageing results in aberrant urothelial function, increased afferent mechanosensitivi

253 logic alterations, with male mice developing urothelial hyperplasia and female mice developing kerati

254 ted novel functions of LIN7C and ARHGAP12 in urothelial integrity and confirmed the essential role of

255 Defects in urothelial integrity resulting in leakage and activation

256 thesis that HA treatment altered the bladder urothelial layer and the expression of hyaluronan-metabo

257 ased the expression of hyaluronidases in the urothelial layer of bladder, resulting in enhanced mucos

258 s, enhance mucosal regeneration, and improve urothelial lining defects in KIC.

259 al differentiation, which might attribute to urothelial lining defects.

260 MA% associated with higher risk of all-site, urothelial, lung, and skin cancers.

261 , and further suggest an epigenetic basis of urothelial maintenance and regeneration.

262 s culminating in end-stage renal failure and urothelial malignancy.

263 the internal tubular urethra was absent, and urothelial morphology and organization was abnormal.

264 14-positive basal cells in the hyperplastic urothelial mucosa in male Foxa1 knockout mice.

265 racts with mannosylated glycoproteins on the urothelial mucosa.

266 s well as in low- and high-grade noninvasive urothelial neoplasms (mean: 74%).

267 nscriptase (hTERT)-immortalized normal human urothelial (NHU) and bladder cancer cell lines to agents

268 erentiation of non-immortalised normal human urothelial (NHU) cells grown in culture.

269 In mouse urothelial organoids, PPAR agonism is sufficient to driv

270 ical control of micturition and suggest that urothelial pannexin may be a viable target for the treat

271 Because PTEN deficiency is cooperative in urothelial pathogenesis, we engineered BHPrE cells with

272 ght junction formation, leading to increased urothelial permeability in bladder pain syndrome.

273 en miR-199a-5p expression and the control of urothelial permeability in bladder pain syndrome.

274 ole of PALS1 in establishing and maintaining urothelial polarity and junction assembly.

275 loss of SPARC accelerated the development of urothelial preneoplasia (atypia and dysplasia), neoplasi

276 epigenetic mechanism by which PRC2 controls urothelial progenitor cell fate and the timing of differ

277 Of note, a key study on urothelial progenitor cells recently highlighted an impo

278 this study, we show that without Sec10, the urothelial progenitor cells that line the ureter fail to

279 rstanding of the origin of this disease from urothelial progenitor cells via field effects along papi

280 iferative and regenerative capacity of adult urothelial progenitors and prevents precocious different

281 d, the obligatory subunit of PRC2, embryonic urothelial progenitors demonstrate reduced proliferation

282 epigenetic regulators in embryonic and adult urothelial progenitors.

283 This was, however, not accompanied by urothelial proliferation or tumorigenesis over 12 months

284 tcomes were any cancer and specific cancers (urothelial, prostate, breast, lung, and colorectal).

285 We further show that response of the urothelial stem cell niche to infection, normally activa

286 Now, using transcriptome analysis in urothelial TEU-2 cells, we implicate it in the regulatio

287 the presence of pannexin 1 and 2 mRNA in rat urothelial tissue, whereas immunofluorescence experiment

288 prostate epithelial cells (BHPrEs) promotes urothelial transdifferentiation.

289 age-related changes in detrusor function and urothelial transmitter release but few studies have inve

290 It has the advantage of minimising urothelial trauma and also helps in assessing any previo

291 Analysis of three independent urothelial tumor cohorts demonstrates a strong associati

292 gs demonstrate an important role for CD24 in urothelial tumorigenesis and metastasis in male mice and

293 llaborate with other genetic events to drive urothelial tumorigenesis.

294 g that the FGFR3 mutations have very limited urothelial tumorigenicity and that these mutations must

295 previously identified as highly relevant in urothelial tumors.

296 e urinary tract in patients at high risk for urothelial tumors.

297 s, characterized by chronic inflammation and urothelial ulceration.

298 luminal surface of terminally differentiated urothelial umbrella cells is almost completely covered b

299 sure in human embryonic kidney (HEK293T) and urothelial (UROtsa) cells to characterize the alteration

300 We conclude that urothelial, VNUT-dependent ATP exocytosis is involved in