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1 on markers and novel therapeutic targets for invasive bladder cancer.
2 gnature to predict progression in non-muscle-invasive bladder cancer.
3 tential prognostic and therapeutic value for invasive bladder cancer.
4 romboxane synthase (TXAS) gene expression in invasive bladder cancer.
5 emains the gold standard for treating muscle-invasive bladder cancer.
6 cal mainstay for the treatment of non-muscle-invasive bladder cancer.
7 ed significant independent associations with invasive bladder cancer.
8 ectomy remains the gold-standard therapy for invasive bladder cancer.
9 cial component of the surgical management of invasive bladder cancer.
10 current radiotherapy in patients with muscle-invasive bladder cancer.
11 ion of severe dysplasia/carcinoma in situ to invasive bladder cancer.
12 upport the aggressive surgical management of invasive bladder cancer.
13 five cystectomy specimens from patients with invasive bladder cancer.
14 t effective therapy for high-risk non-muscle-invasive bladder cancer.
15 f life of patients undergoing cystectomy for invasive bladder cancer.
16 apy over radical cystectomy alone for muscle-invasive bladder cancer.
17 and BM staining as prognostic indicators in invasive bladder cancer.
18 servation in the management of patients with invasive bladder cancer.
19 ve harnessed for the treatment of non-muscle-invasive bladder cancer.
20 ent and the protocol for treating non-muscle invasive bladder cancer.
21 tment of both non-muscle-invasive and muscle-invasive bladder cancer.
22 Calmette-Guerin (BCG)-experienced non-muscle-invasive bladder cancer.
23 dvanced solid malignancies, including muscle-invasive bladder cancer.
24 ade nonmuscle-invasive and high-grade muscle-invasive bladder cancer.
25 ineligible patients with cT2-4aN0-1M0 muscle-invasive bladder cancer.
26 -1 inhibitor, in BCG-unresponsive non-muscle-invasive bladder cancer.
27 onal character found in patients with muscle-invasive bladder cancer.
28 edanib or placebo in locally advanced muscle-invasive bladder cancer.
29 for cisplatin-eligible patients with muscle-invasive bladder cancer.
30 in patients with BCG-unresponsive non-muscle-invasive bladder cancer.
31 d survival evaluated in patients with muscle invasive bladder cancer.
32 in approximately 40% of patients with muscle-invasive bladder cancer.
33 hemotherapy and radical treatment for muscle-invasive bladder cancer.
34 of recurrence and progression of non-muscle-invasive bladder cancer.
35 enefits to anti-PD-1 treatment in non-muscle invasive bladder cancer.
36 of pathological complete response in muscle-invasive bladder cancer.
37 or cisplatin-ineligible patients with muscle-invasive bladder cancer.
38 lity therapy for select patients with muscle-invasive bladder cancer.
39 elective bladder-sparing treatment of muscle-invasive bladder cancer.
40 spheroids derived from patients with muscle-invasive bladder cancer.
41 red from toenails and the risk of non-muscle invasive bladder cancer.
42 motherapy on response and survival in muscle-invasive bladder cancer.
43 in patients with BCG-unresponsive non-muscle-invasive bladder cancer.
44 change management of patients with nonmuscle invasive bladder cancer.
45 NAs to help evaluate patients with nonmuscle invasive bladder cancer.
46 ladder preservation for patients with muscle invasive bladder cancer.
47 urrent use with radiotherapy to treat muscle-invasive bladder cancer.
48 ve the cure rates of patients diagnosed with invasive bladder cancer.
49 podia of angiogenic endothelial tip cells in invasive bladder cancer.
50 hemotherapy regimen for patients with muscle invasive bladder cancer.
51 h metastatic disease in patients with muscle-invasive bladder cancer.
52 native to cystectomy in patients with muscle-invasive bladder cancer.
53 ical therapy for BCG-unresponsive non-muscle-invasive bladder cancer.
54 verall survival after radical cystectomy for invasive bladder cancer.
55 cystectomy or radiotherapy alone, for deeply invasive bladder cancer.
56 tcome as first-line adjunctive treatment for invasive bladder cancer.
57 from controls and also nonmuscle from muscle-invasive bladder cancer.
58 tcomes and quality of life for patients with invasive bladder cancer.
59 ection (PLND) is the preferred treatment for invasive bladder cancer.
60 u (CIS), the precursor lesion of most muscle-invasive bladder cancers.
61 atment for localized and regionally advanced invasive bladder cancers.
62 resented both superficial bladder tumors and invasive bladder cancers.
63 inoma (mUC), and as high as 80% in nonmuscle invasive bladder cancers.
64 ers, and (3) PGDH is completely lost in most invasive bladder cancers.
65 Of 432 newly evaluated patients with muscle-invasive bladder cancer, 151 were treated by standard ra
67 s or older, with BCG-unresponsive non-muscle-invasive bladder cancer and an Eastern Cooperative Oncol
69 its applicability in case studies of muscle-invasive bladder cancer and essential thrombocythemia.
70 is the cornerstone treatment for non-muscle-invasive bladder cancer and intravesical therapy can fur
72 ve been identified in up to 15-20% of muscle-invasive bladder cancer and metastatic urothelial carcin
73 fered to all suitable candidates with muscle-invasive bladder cancer and not only to patients with si
74 receptor I (IGF-IR) is up-regulated in human invasive bladder cancer and promotes migration and invas
75 nts completing combined-modality therapy for invasive bladder cancer and retaining their native bladd
76 ant role in non-invasive than that in muscle-invasive bladder cancer and suggest that cohesin complex
77 he definition of BCG-unresponsive non-muscle-invasive bladder cancer and were therefore excluded from
78 on definition of BCG-unresponsive non-muscle-invasive bladder cancer and were therefore not included
79 ing intermediate, were present in high-grade invasive bladder cancers and associated with more freque
80 el to help predict progression of non-muscle-invasive bladder cancers and delineate a systematic, gen
81 marker in 81% of human high-grade nonmuscle invasive bladder cancers and used as a target for the de
82 mainstay definitions of high-risk nonmuscle invasive bladder cancer are based on grade and stage.
85 aring many of the genetic features of muscle-invasive bladder cancers, are classified as non-muscle-i
86 oma of the urinary bladder (a model of human invasive bladder cancer) as well as adjacent normal tiss
87 ell, and squamous cell carcinoma subtypes of invasive bladder cancer, as well as in T24, J82, and UM-
89 for muscle-invasive and high-risk nonmuscle-invasive bladder cancer (BCa), but is associated with si
92 ign and interpretation of clinical trials in invasive bladder cancer but also help to identify and op
93 surgery achieve similar cure rates in muscle-invasive bladder cancer, but the choice of which treatme
94 we created a novel transgenic mouse model of invasive bladder cancer by targeting an active dimerized
96 ubstrate (HA)-gel technique, showed that the invasive bladder cancer cell lines secrete elevated leve
97 proteome of the RT4 non-invasive and HT1197 invasive bladder cancer cell lines was identified and in
98 eport a comprehensive analysis of 412 muscle-invasive bladder cancers characterized by multiple TCGA
99 servation with radical cystectomy for muscle-invasive bladder cancer closed due to insufficient accru
101 ectomy is the preferred treatment for muscle-invasive bladder cancer despite modest survival benefit
104 Patients with clinical T2-4aN0/XM0 muscle-invasive bladder cancer eligible for RC were enrolled.
106 kers may have prognostic value in non-muscle invasive bladder cancer for guiding optimal treatment of
108 itulates this unique clinical progression of invasive bladder cancer has not yet been developed.
109 umors, several histopathological subtypes of invasive bladder cancer have been identified as being mo
110 Patients with locally 'advanced' or muscle invasive bladder cancer have higher mortality rates than
111 tment for patients with high-risk non-muscle-invasive bladder cancer (HR-NMIBC) is tumor resection fo
115 dder cancer (NMIBC), high-risk NMIBC, muscle-invasive bladder cancer in the neoadjuvant and adjuvant
121 n increasingly common malignancy, and muscle invasive bladder cancer is associated with particularly
123 Standard treatment for high-risk non-muscle-invasive bladder cancer is transurethral resection of bl
124 cystectomy and urinary diversion for muscle invasive bladder cancer), kidney surgery (nephrectomy, d
125 cantly associated with progression to muscle-invasive bladder cancer (log-rank test; P < 0.001) in th
128 ded to accurately stage patients with muscle-invasive bladder cancer (MIBC) and metastatic urothelial
131 The current treatment paradigm for muscle-invasive bladder cancer (MIBC) consists of cisplatin-bas
135 their urinary bladder despite having muscle-invasive bladder cancer (MIBC) has sparked years of rese
136 omy (RC) for definitive management of muscle-invasive bladder cancer (MIBC) in current clinical guide
138 the immune microenvironment of cancer.Muscle-invasive bladder cancer (MIBC) is a potentially lethal d
141 r, clinical response in patients with muscle-invasive bladder cancer (MIBC) is limited, with only 20-
142 The standard of care treatment for muscle-invasive bladder cancer (MIBC) is radical cystectomy, wh
144 e method of assessing the response of muscle-invasive bladder cancer (MIBC) to neoadjuvant treatment
145 adiation is debated for patients with muscle-invasive bladder cancer (MIBC) undergoing curative-inten
146 o radical cystectomy for treatment of muscle-invasive bladder cancer (MIBC), but biomarkers are neede
147 ystectomy is a standard treatment for muscle-invasive bladder cancer (MIBC), but it is life-altering.
148 ing trials of neoadjuvant therapy for muscle-invasive bladder cancer (MIBC), identifying opportunitie
149 is viewed as the standard of care for muscle-invasive bladder cancer (MIBC), radiotherapy-based, blad
150 g combined-modality therapy (CMT) for muscle-invasive bladder cancer (MIBC), reserving cystectomy for
152 ne-excluded syngeneic mouse models of muscle-invasive bladder cancer (MIBC), we show that platinum-ba
160 chemotherapy is standard of care for muscle-invasive bladder cancer (MIBC); however, it is infrequen
167 ) patients received mBCG, four had nonmuscle invasive bladder cancer (NMIBC) after induction, three h
168 dder cancer improves detection of non-muscle-invasive bladder cancer (NMIBC) and reduces recurrence r
169 Once diagnosed, patients with nonmuscle invasive bladder cancer (NMIBC) are committed to a lifet
170 pose Many patients with high-risk non-muscle-invasive bladder cancer (NMIBC) are either refractory to
172 rexpression of fibulin-3 in T2 vs non-muscle-invasive bladder cancer (NMIBC) by quantitative reverse
174 care for patients with high-risk non-muscle-invasive bladder cancer (NMIBC) for several decades.
175 PURPOSE OF REVIEW: As high-risk nonmuscle invasive bladder cancer (NMIBC) has a high propensity to
176 It has long been recognized that non-muscle-invasive bladder cancer (NMIBC) has a low propensity (20
184 ion of EV mRNA markers to monitor non-muscle invasive bladder cancer (NMIBC) recurrence after TURBT.
188 mic profiling of premalignant and non-muscle invasive bladder cancer (NMIBC) that ensued in the chemi
189 mited for patients with high-risk non-muscle-invasive bladder cancer (NMIBC) with disease recurrence
190 with intermediate- and high-risk non-muscle-invasive bladder cancer (NMIBC) without carcinoma in sit
191 the current standard of care for non-muscle-invasive bladder cancer (NMIBC), but recurrence is commo
192 dies in low- and intermediate-risk nonmuscle-invasive bladder cancer (NMIBC), high-risk NMIBC, muscle
193 cancer is primarily diagnosed as non-muscle-invasive bladder cancer (NMIBC), with high recurrence an
201 nge was associated with lower odds of muscle-invasive bladder cancer (odds ratio [OR], 0.91; 95% CI,
202 a 1:1 ratio, patients with localized muscle-invasive bladder cancer of clinical stage T2 (confined t
203 omprised genes frequently affected in muscle-invasive bladder cancer of nonpapillary origin, focusing
204 isease-free survival of high-risk non-muscle-invasive bladder cancer or progressive disease as assess
205 sponse rate (absence of high-risk non-muscle-invasive bladder cancer or progressive disease), assesse
206 In summary, these data support a model of invasive bladder cancer pathogenesis in which both the p
207 1, an aggressive cisplatin-resistant muscle-invasive bladder cancer patient-derived xenograft (PDX)
208 nalysis provides prognostic value for muscle invasive bladder cancer patients and a better model fit
211 stigation of TAR-200 in patients with muscle-invasive bladder cancer planned for radical cystectomy.
212 re, we profile the global proteome of muscle-invasive bladder cancers pre- and post-neoadjuvant chemo
214 nagement strategies for low-grade non-muscle invasive bladder cancer rely heavily on routine office c
217 -12-82 GG polymorphisms were associated with invasive bladder cancer risk [odds ratio (OR), 2.60; 95%
219 eatments are needed for patients with muscle-invasive bladder cancer scheduled for radical cystectomy
221 agnosed with histologically confirmed muscle-invasive bladder cancer (stage cT2-cT4 N0M0), had an Eas
222 Patients were enrolled if they had muscle-invasive bladder cancer (stage T2 to T4a) and were to be
224 ations are frequent genomic events in muscle-invasive bladder cancer (TCGA bladder cancer data set: a
226 so shown to localize to the nucleus of human invasive bladder cancers that were primarily composed of
229 py for intermediate and high-risk non-muscle-invasive bladder cancer, the therapeutic options for mus
231 nstrated that the IGF-IR is overexpressed in invasive bladder cancer tissues and promotes motility an
232 nstrated that the IGF-IR is overexpressed in invasive bladder cancer tissues compared with nonmaligna
233 tio, cisplatin-eligible patients with muscle-invasive bladder cancer to receive neoadjuvant durvaluma
234 e randomly assigned 360 patients with muscle-invasive bladder cancer to undergo radiotherapy with or
235 n frozen tumor samples from 42 patients with invasive bladder cancer treated by cystectomy with monoc
236 overall survival among patients with muscle-invasive bladder cancer undergoing radical cystectomy an
237 ectomy, among patients with localized muscle-invasive bladder cancer undergoing radical cystectomy is
238 monotherapy for treating high-risk nonmuscle invasive bladder cancer unresponsive to bacillus Calmett
239 in cisplatin-ineligible patients with muscle-invasive bladder cancer, warranting additional study as
240 emotherapy does benefit patients with muscle-invasive bladder cancer, we reviewed all phase II and II
242 s of ET-1 are higher in patients with muscle-invasive bladder cancers, which are associated with high
243 in patients with BCG-unresponsive non-muscle-invasive bladder cancer who declined or were ineligible
244 ologic reports from 268 patients with muscle-invasive bladder cancer who received radical cystectomy.
245 s with BCG-unresponsive high-risk non-muscle-invasive bladder cancer who were ineligible for or decli
246 in patients with BCG-unresponsive non-muscle-invasive bladder cancer with carcinoma in situ (CIS).
247 les of blood vascular endothelium from human invasive bladder cancer with normal bladder tissue, we f
248 nd had BCG-unresponsive high-risk non-muscle-invasive bladder cancer with papillary tumours (high-gra
249 er is the highest risk subtype of non-muscle-invasive bladder cancer with unpredictable outcome and p
251 ture, which effectively distinguishes muscle-invasive bladder cancer with worse clinical prognosis fr
252 lysed p73 mutations in 23 unselected primary invasive bladder cancers with matched normal tissues and
253 er is the highest risk subtype of non-muscle-invasive bladder cancer, with highly variable prognosis,
254 ajor treatment modality used to treat muscle-invasive bladder cancer, with patient outcomes similar t
255 bladder epithelial HCV29 cells versus highly invasive bladder cancer YTS1 cells, both derived from tr