ライフサイエンスコーパス: urothelial

1 t common primary tumors were breast (33.3%), urothelial (12.5%), and cervical cancer (10.4%).Grade 3

2 evealed significant edema and alterations of urothelial architecture in RUTI patient biopsies.

3 ion between severe urocystitis with reactive urothelial atypia and carcinoma in situ (CIS) can be dif

4 Reactive urothelial atypia and CIS were distinguishable on the ba

5 AHNAK2 can differentiate between reactive urothelial atypia in the setting of an acute or chronic

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

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

8 seen in forms of cystitis that coexist with urothelial barrier dysfunction could be alleviated by cu

9 ctly regulate detrusor contractility and the urothelial barrier function.

10 Abnormalities in the urothelial barrier have been described in certain forms

11 ells, which are critical for maintaining the urothelial barrier, fail to mature in Pparg mutants and

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

13 d therefore facilitates our understanding of urothelial biology.

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

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

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

17 t urothelial cancer subtypes, as well as non-urothelial bladder cancers, and discuss how the integrat

18 d ratio (HR) = 0.71 [0.60-0.85], p = 0.0002, urothelial bladder carcinoma: HR = 0.74 [0.59-0.93], p =

19 patients with muscle-invasive and metastatic urothelial cancer (interpatient heterogeneity) probably

20 current biopsy-proven, low-grade upper tract urothelial cancer (measuring 5-15 mm in maximum diameter

21 Background Muscle-invasive urothelial cancer (MIUC) is characterized by substantial

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

23 equences of deleterious germline variants in urothelial cancer (UC) are not fully characterized.

24 CLC, 33% (7/21; 95% CI, 14.6% to 57.0%); and urothelial cancer 25% (5/20; 95% CI, 8.7% to 49.1%).

25 Patients with metastatic urothelial cancer achieving at least stable disease on f

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

27 Most patients with low-grade upper tract urothelial cancer are treated by radical nephroureterect

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

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

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

31 e increased risks of hemorrhagic cystitis or urothelial cancer from persistent and ectopic KRT14(+) c

32 clusion Mutational status of muscle-invasive urothelial cancer has implications on metastatic pattern

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

34 erapy for first-line treatment of metastatic urothelial cancer is typically administered for a fixed

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

36 ement of conventional, variant and divergent urothelial cancer subtypes, as well as non-urothelial bl

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

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

39 imary chemoablation of low-grade upper tract urothelial cancer with intracavitary UGN-101 results in

40 response in a spectrum of tumors, including urothelial cancer(4-7).

41 motherapy versus sUrveillance in upper Tract urothelial cancer) trial aimed to assess the efficacy of

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

43 er, four (25%, 7.3-52.4) of 16 patients with urothelial cancer, and five (39%, 13.9-68.4) of 13 patie

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

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

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

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

48 hemorrhagic cystitis and eventually bladder urothelial cancer.

49 l protein 72 as a biomarker for prognosis of urothelial cancer.

50 noma, non-small-cell lung cancer (NSCLC), or urothelial cancer.

51 1-amplified sqNSCLC and FGFR3-mutant bladder/urothelial cancer.

52 ally advanced and unresectable or metastatic urothelial cancer.

53 patients with locally advanced or metastatic urothelial cancer.

54 its therapeutic use in untreated metastatic urothelial cancer.

55 istent with locally recurrent and metastatic urothelial cancer.

56 its therapeutic use in untreated metastatic urothelial cancer.

57 on-free survival in patients with metastatic urothelial cancer.

58 Urothelial cancers (UCs) have a substantial hereditary c

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

60 es differed among histologies (eg, > 35% for urothelial cancers and < 6% for pancreatic and small-cel

61 Urothelial cancers are amongst the 10 most common types

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

63 great efficacy in a proportion of metastatic urothelial cancers(1,2).

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

65 1-amplified sqNSCLC and FGFR3-mutant bladder/urothelial cancers.

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

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

68 set of genome-wide epigenetic aberrations in urothelial carcinogenesis.

69 ), non-small-cell lung cancer (cohort C), or urothelial carcinoma (cohort D), whose disease had progr

70 representing 1,445 patients with metastatic urothelial carcinoma (mUC) and metastatic renal cell car

71 ab (CaboNivoIpi) in patients with metastatic urothelial carcinoma (mUC) and other genitourinary (GU)

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

73 unresectable locally advanced or metastatic urothelial carcinoma (mUC) treated with nivolumab 3 mg/k

74 f 27 patients), and colitis in patients with urothelial carcinoma (two [8%] of 24 patients).

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

76 ninvasive urine test has become the goal for urothelial carcinoma (UC) diagnosis and surveillance.

77 ecognized as a potential oncogenic factor of urothelial carcinoma (UC) in renal transplant recipients

78 Urothelial carcinoma (UC) is a common disease causing si

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

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

81 advanced or metastatic cisplatin-ineligible urothelial carcinoma (UC).

82 ment paradigms for patients with upper tract urothelial carcinoma (UTUC) are typically extrapolated f

83 Upper tract urothelial carcinoma (UTUC) is characterized by a distin

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

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

86 in-4-expressing solid tumors (eg, metastatic urothelial carcinoma [mUC]) who progressed on >= 1 prior

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

88 rmed in three patients with BKPyV-associated urothelial carcinoma after renal transplantation.

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

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

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

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

93 morphological characteristics divergent from urothelial carcinoma are extreme examples of tumour hete

94 Patients with metastatic urothelial carcinoma are often ineligible for cisplatin-

95 ociated antigen found on the surface of most urothelial carcinoma cells.

96 ded in all four expansion cohorts (12 in the urothelial carcinoma cohort and one in each of the other

97 cer cohort, and three (13%, 2.7-32.4) in the urothelial carcinoma cohort.

98 of the bladder (LELC-B) is a rare subtype of urothelial carcinoma consisting of undifferentiated epit

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

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

101 the tumor is the first line of treatment for urothelial carcinoma in situ (CIS), the precursor lesion

102 -cell clones also give rise to both SCCB and urothelial carcinoma in xenografts.

103 Locally advanced or metastatic urothelial carcinoma is an incurable disease with limite

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

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

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

107 Urothelial carcinoma is the most common type of bladder

108 Urothelial carcinoma is the most common type of bladder

109 Urothelial carcinoma may be classified as either immune

110 nrolled in parallel (patients with bone-only urothelial carcinoma metastases and patients with rare h

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

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

113 owth factor receptor 3 (FGFR3) are common in urothelial carcinoma of the bladder (UC).

114 In urothelial carcinoma of the bladder (UCB), silencing of

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

116 Metastatic urothelial carcinoma of the bladder is generally incurab

117 tment-naive advanced or recurrent metastatic urothelial carcinoma of the bladder, ureter, or urethra

118 ized by a lower total mutational burden than urothelial carcinoma of the bladder.

119 Histological and molecular analyses of urothelial carcinoma often reveal intratumoural and inte

120 years or older, had histologically confirmed urothelial carcinoma or rare genitourinary tract histolo

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

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

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

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

125 SCCB model and a cohort of patient SCCB and urothelial carcinoma samples to characterize molecular s

126 Cystitis and invasive high-grade urothelial carcinoma samples were analyzed.

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

128 istry in a small cohort, including low-grade urothelial carcinoma samples.

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

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

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

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

133 and anti-PDL1 immunotherapy has transformed urothelial carcinoma treatment.

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

135 atients with previously untreated metastatic urothelial carcinoma who benefit from treatment with imm

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

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

138 tcomes are poor for patients with metastatic urothelial carcinoma who receive standard, first-line, p

139 patients with locally advanced or metastatic urothelial carcinoma who were previously treated with pl

140 patients with locally advanced or metastatic urothelial carcinoma who were previously treated with pl

141 patients with locally advanced or metastatic urothelial carcinoma who were previously treated with pl

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

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

144 y pretreated, platinum-refractory metastatic urothelial carcinoma with measurable disease and bone me

145 Cohort one included patients with metastatic urothelial carcinoma with measurable disease as defined

146 ded if they had upper urinary tract disease, urothelial carcinoma within the prostatic urethra, lymph

147 adjuvant setting for patients with localized urothelial carcinoma(1,2), with one study reporting data

148 or those with non-small-cell lung cancer and urothelial carcinoma) that included platinum (for all tu

149 with non-small-cell lung cancer, and 24 with urothelial carcinoma).

150 d appetite and diarrhoea in one patient with urothelial carcinoma, and acute kidney injury [NSCLC], h

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

152 phenotypes, including small cell carcinoma, urothelial carcinoma, and squamous cell carcinoma.

153 unresectable, locally advanced or metastatic urothelial carcinoma, conducted at 224 academic research

154 RNA-overexpressing tumours [52 patients with urothelial carcinoma, eight patients with HNSCC, 20 pati

155 ther development for patients with localized urothelial carcinoma, especially cisplatin-ineligible pa

156 or older with locally advanced or metastatic urothelial carcinoma, from 221 sites in 35 countries, we

157 e for expansion to patients in four cohorts: urothelial carcinoma, head and neck squamous-cell cancer

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

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

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

161 on-free survival in patients with metastatic urothelial carcinoma.

162 administered to 125 patients with metastatic urothelial carcinoma.

163 rgets Nectin-4, which is highly expressed in urothelial carcinoma.

164 r patients with platinum-refractory advanced urothelial carcinoma.

165 nocarcinoma, non-small-cell lung cancer, and urothelial carcinoma.

166 enocarcinoma, non-small-cell lung cancer, or urothelial carcinoma.

167 patients with metastatic platinum-refractory urothelial carcinoma.

168 body, in patients with refractory metastatic urothelial carcinoma.

169 s with metastatic or surgically unresectable urothelial carcinoma.

170 n patients with platinum-refractory advanced urothelial carcinoma.

171 erapeutic treatment option for patients with urothelial carcinoma.

172 h platinum-refractory advanced or metastatic urothelial carcinoma.

173 patients with locally advanced or metastatic urothelial carcinoma.

174 igation of nivolumab monotherapy in advanced urothelial carcinoma.

175 patients with locally advanced or metastatic urothelial carcinoma.

176 ee survival in platinum-refractory, advanced urothelial carcinoma.

177 patients with locally advanced or metastatic urothelial carcinoma.

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

179 motherapy in locally advanced and metastatic urothelial carcinoma.

180 equired to improve survival of patients with urothelial carcinoma.

181 patients with locally advanced or metastatic urothelial carcinoma.

182 l first-line treatment option for metastatic urothelial carcinoma.

183 r), as a first-line treatment for metastatic urothelial carcinoma.

184 -based chemotherapy in first-line metastatic urothelial carcinoma.

185 can induce sustained responses in metastatic urothelial carcinoma.

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

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

188 opathy [urothelial carcinoma], and vomiting [urothelial carcinoma] in one patient each); no treatment

189 lycaemia [other solid tumours], retinopathy [urothelial carcinoma], and vomiting [urothelial carcinom

190 patients with MPBC-HGT1 and 64 conventional urothelial carcinomas (cUC) (reference set) was performe

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

192 The study utilized a series of urothelial carcinomas (UCs) by tissue microarray, on whi

193 Urothelial carcinomas of the upper urinary tract (UTUCs)

194 , with poorer stage-for-stage prognosis than urothelial carcinomas of the urinary bladder.

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

196 n in renal clear cell carcinomas and bladder urothelial carcinomas, tumors associated with TSC gene m

197 ure can define MPBC-HGT1 within conventional urothelial carcinomas.

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

199 Accurate grading of non-muscle-invasive urothelial cell carcinoma is of major importance; howeve

200 the fully automated detection and grading of urothelial cell carcinoma.

201 TP to act in an autocrine manner, modulating urothelial cell function.

202 quantified the effects of exogenous IL-4 on urothelial cell proliferation in vitro, including cell c

203 ise the functional response of primary mouse urothelial cells (PMUCs) to ATP.

204 14(+) (KRT14(+)) basal progenitors or other urothelial cells 1 day after cyclophosphamide exposure.

205 re work to identify the interactions between urothelial cells and sensory neurons that control urinat

206 histosome eggs promoted proliferation of the urothelial cells but inhibited growth of cholangiocytes.

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

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

209 Urothelial cells contribute to bladder functions, includ

210 er bladder cancer phenotypes by showing that urothelial cells driven by a set of defined oncogenic fa

211 lation of estrogen receptor was predicted in urothelial cells exposed only to S. haematobium eggs.

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

213 This method can isolate single urothelial cells for electrophysiology in situ and can a

214 Here we show that Pparg is critical in urothelial cells for mitochondrial biogenesis, cellular

215 percentage of UPEC binding or invading human urothelial cells increased; when cells overexpressed RNa

216 Most methods of isolating urothelial cells require enzymes; however, these techniq

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

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

219 Functional studies of urothelial cells usually use either freshly isolated cel

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

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

222 ly deliver high concentrations of drugs into urothelial cells, and have the potential to be a more ef

223 properties of the urothelium (e.g. cultured urothelial cells, bladder mucosa sheets mounted in Ussin

224 Studies of urothelial cells, bladder sheets or lumens of filled bla

225 -cell and cell-matrix adhesion properties of urothelial cells, resulting in loss of contact-inhibitio

226 7's antimicrobial activity in vitro in human urothelial cells, we used siRNA to silence urothelial RN

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

228 transformation of nonmalignant human SV-HUC urothelial cells.

229 ucosa or whole bladder do not represent pure urothelial cells.

230 effects in human lung epithelial and bladder urothelial cells.

231 abetic metabolites activate NLRP3 in primary urothelial cells.

232 er Ca(2+) rise than purinergic activation in urothelial cells.

233 lls, but not in the less glycosylated benign urothelial cells.

234 , we identified genomic alterations (GAs) in urothelial CIS having the potential to predict response

235 de a basis for future mechanistic studies of urothelial CIS pathogenesis.

236 expanding and sustaining the accumulation of urothelial CSCs.

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

238 Conditional urothelial deletion of Fgfr2 (Fgfr2KO) did not affect in

239 hat CAKUTs can arise as a result of abnormal urothelial development.

240 The nuclear receptor Pparg promotes urothelial differentiation in vitro, and Pparg mutations

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

242 Urothelial exposure to IL-4 in vitro led to cell cycle p

243 The mechanisms underlying urothelial formation and maintenance are largely unknown

244 thelial proliferation, including evidence of urothelial hyper-diploidy and cell cycle skewing in wild

245 carcinomas (9 of 40 mice, 22.5%) and bladder urothelial hyperplasia (23 of 40 mice, 57.5%).

246 A range of pathology occurs, including urothelial hyperplasia and cancer, but associated mechan

247 ession of Upk2-HRAS* oncogene, an inducer of urothelial hyperplasia in transgenic mice.

248 Our results indicate that maintenance of urothelial hyperplasia in Upk2-HRAS* mice depends on con

249 ECS induces lung adenocarcinomas and bladder urothelial hyperplasia, combined with our previous findi

250 effectors may mediate oncogene addiction in urothelial hyperplasia.

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

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

253 GFRalpha(+) cells present in adventitial and urothelial layers of murine renal pelvis do not express

254 ttle proliferation and marked restoration of urothelial layers, whereas the phosphate-buffered saline

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

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

257 tocols, it does not require debriding of the urothelial lining, injection into the bladder wall, spec

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

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

260 nit 4) and examined its potential in imaging urothelial malignancies.

261 f the molecular alterations occurring during urothelial malignant transformation and indicates TAZ as

262 understanding of how FGFR3 activation drives urothelial malignant transformation remains limited.

263 pithelia displaying robust expression of the urothelial marker uroplakin.

264 racts with mannosylated glycoproteins on the urothelial mucosa.

265 The invasion of bladder cancer into the sub-urothelial muscle and vasculature are key determinants l

266 nflammation induces bladder overactivity and urothelial NGF overexpression in the bladder, both depen

267 aged 18 years or older with breast, gastric, urothelial, or endometrial cancer with at least HER2 imm

268 Using a human urothelial organoid model, we tested the ability of nove

269 Urothelial organoids provide a powerful tool to study ce

270 Here, we establish mouse urothelial organoids that can be maintained uninterrupte

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

272 We demonstrate that SCCB shares a urothelial origin with other bladder cancer phenotypes b

273 Despite this shared urothelial origin, clinical SCCB samples have a distinct

274 bladder hyperactivity in rats with increased urothelial permeability.

275 that forms paracellular pores and increases urothelial permeability.

276 burothelium, and bladder smooth muscle, with urothelial predominance.

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

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

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

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

281 epigenetic regulators in embryonic and adult urothelial progenitors.

282 proliferation, decreased cell layer number, urothelial program activation, and acquisition of barrie

283 This led to a marked reduction of urothelial proliferation as evidenced by urothelial thin

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

285 bladder histology and ex vivo assessments of urothelial proliferation, cell cycle, and ploidy status.

286 matobium egg injection triggered significant urothelial proliferation, including evidence of urotheli

287 66) had tumors other than CRC/EC, including urothelial, prostate, pancreas, adrenocortical, small bo

288 RT14(-) cell proliferation, leading to early urothelial regeneration.

289 ongenital urinary tract obstruction triggers urothelial remodelling that stabilizes the obstructed ki

290 2/ERK signaling apparently leads to abnormal urothelial repair after cyclophosphamide exposure from p

291 ngle cell RT-PCR, while sensory neuronal and urothelial responses to 5-HT were determined by live cel

292 n urothelial cells, we used siRNA to silence urothelial RNase 7 production and retroviral constructs

293 t stretch evoked significant ATP release-key urothelial sensory process, from live mucosa tissue, ful

294 Understanding urothelial stem cell biology and differentiation has bee

295 of urothelial proliferation as evidenced by urothelial thinning, degenerative changes such as intrac

296 physiology in situ and can also isolate pure urothelial tissue for PCR, microarray, and immunoblot pr

297 The time required to obtain urothelial tissue from one mouse bladder is 15-20 min.

298 t require enzymes and is able to obtain pure urothelial tissues from mice and humans.

299 rease in cancer states of breast, kidney and urothelial tissues, but not in lung.

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

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

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

303 genic bacteria have been shown to invade the urothelial wall during acute UTI, forming latent intrace