ライフサイエンスコーパス: prostate cancer

1 Diagnosis with favorable-risk prostate cancer.

2 omising results for the diagnostic workup of prostate cancer.

3 as a strategy to treat castration-resistant prostate cancer.

4 ficacy of paclitaxel in paclitaxel-resistant prostate cancer.

5 herapy (EBRT) with brachytherapy in men with prostate cancer.

6 e prostate (TRAMP) transgenic mouse model of prostate cancer.

7 ervation for men with low-risk and high-risk prostate cancer.

8 d therapy (RLT) is applied in advanced-stage prostate cancer.

9 ate therapeutic target for treating advanced prostate cancer.

10 d should be considered for intermediate-risk prostate cancer.

11 ecedented accuracy for whole-body staging of prostate cancer.

12 man and used parameters for PSA shedding and prostate cancer.

13 effective treatment for low-risk, localised prostate cancer.

14 (98/130) other cancers, and 58.9% (298/506) prostate cancer.

15 olone improves survival in men with relapsed prostate cancer.

16 rapy-naive, metastatic, castration-resistant prostate cancer.

17 nant lesion in patients with newly diagnosed prostate cancer.

18 gnosis, detection, and treatment of invasive prostate cancer.

19 ibitor, in the early treatment of metastatic prostate cancer.

20 atients with metastatic castration-resistant prostate cancer.

21 PTEN activity is often lost in prostate cancer.

22 umor progression in an experimental model of prostate cancer.

23 to 2012, and 192,838 age-matched men free of prostate cancer.

24 l target for the diagnosis and management of prostate cancer.

25 luding Alzheimer's disease, in patients with prostate cancer.

26 egret among long-term survivors of localized prostate cancer.

27 nscriptional signature consistent with human prostate cancer.

28 antitumor activity against hormone-sensitive prostate cancer.

29 ta included 140 patients suspected of having prostate cancer.

30 arative harms of contemporary treatments for prostate cancer.

31 comes dysregulated in primary and metastatic prostate cancer.

32 lar disease, diabetes, testicular cancer, or prostate cancer.

33 to further interrogate the biology of EMT in prostate cancer.

34 of early targeted therapeutic strategies for prostate cancer.

35 or detection and characterization of primary prostate cancer.

36 aying osteoporosis in men with nonmetastatic prostate cancer.

37 a generalized therapeutic approach to manage prostate cancer.

38 ine factor in various malignancies including prostate cancer.

39 atients with metastatic castration-resistant prostate cancer.

40 equired for effective treatment of high risk prostate cancer.

41 c PET tracer in prestaging and monitoring of prostate cancer.

42 state-specific Pten deletion mouse model for prostate cancer.

43 ncer types, as new tumor suppressor genes in prostate cancer.

44 -PSMA-617 RLT in a syngeneic model of murine prostate cancer.

45 ed somatostatin receptor sst5TMD4 variant in prostate cancer.

46 in approximately 30% of castration-resistant prostate cancer.

47 ically relevant androgen regulated target in prostate cancer.

48 d to be overexpressed in ovarian, breast and prostate cancers.

49 pair genes by androgen receptor signaling in prostate cancers.

50 NEK6 was overexpressed in a subset of human prostate cancers.

51 ithelial cells in normal tissues, but not in prostate cancers.

52 erall survival [OS], 69%), followed by basal prostate cancers (10-year bRFS, 39%; DMFS, 73%; PCSS, 86

53 DMFS, 73%; PCSS, 86%; OS, 80%) and luminal A prostate cancers (10-year bRFS, 41%; DMFS, 73%; PCSS, 89

54 agnostic accuracy for clinically significant prostate cancer achieved with abbreviated biparametric p

55 Results Among 31,790 patients, 7,365 died of prostate cancer and 11,811 died from other causes during

56 Eligible patients had metastatic prostate cancer and a PSA level higher than 4.0 ng/mL be

57 ported on various cancer types, for example, prostate cancer and breast cancer, targeting this recept

58 23)RaCl2 therapy of patients with metastatic prostate cancer and its impact on the therapeutic respon

59 th neoplastic diseases such as colon cancer, prostate cancer and neuroblastoma.

60 Mechanistic studies of deregulated ERG in prostate cancer and other cancers continue to enhance it

61 at enzalutamide treatment in human models of prostate cancer and patient tissues is accompanied by a

62 24% of disparities in breast cancer, 24% in prostate cancer, and 16% to 30% in colorectal cancer.

63 of bone mass, chronic diseases, skin cancer, prostate cancer, and cardiovascular disease.

64 creased PI(3,4)P2 levels in a mouse model of prostate cancer, and it inversely correlated with PI(3,4

65 eneity in a 38-dimensional network model for prostate cancer, and provide a new strategy on controlli

66 (GRPr) are frequently overexpressed in human prostate cancer, and radiolabeled GRPr affinity ligands

67 compared to primary and castration-resistant prostate cancers, and its expression is negatively corre

68 ssociations between GWAS-identified SNPs and prostate cancer are modified by circulating concentratio

69 aggressive (Gleason score, >/=7) early-stage prostate cancer are undermined by harms from unnecessary

70 nt common and rarer cancers, with breast and prostate cancer as baseline categories for women and men

71 Herein, by using paired normal and prostate cancer-associated stromal fibroblasts (CAFs) de

72 a large cohort of men treated surgically for prostate cancer, associating alterations with biochemica

73 ated with 25(OH)D concentration, and the SNP-prostate cancer associations did not differ by these con

74 ng 95% sensitivity for predicting aggressive prostate cancer at initial biopsy.

75 stance to BET inhibitors in individuals with prostate cancer bearing SPOP mutations.

76 e </= 75 years when diagnosed with localized prostate cancer between October 1994 and October 1995 in

77 sal and correlative association of TFF1 with prostate cancer biology in vitro and in patient specimen

78 promise for monitoring treatment response in prostate cancer bone metastases.

79 affecting the pathogenesis of male-specific prostate cancer but also likely contributing to sex diff

80 association of vitamin D concentrations and prostate cancer, but little is known about whether the a

81 GR expression is silenced in prostate cancer by a combination of AR binding and EZH2-

82 egister of Sweden, which includes all 38,570 prostate cancer cases diagnosed from 2009 to 2012, and 1

83 performed with mice bearing LNCaP and PC-3 (prostate cancer cell line; PSMA-negative) tumors.

84 tested SiNVICT on simulated data as well as prostate cancer cell lines and cfDNA obtained from castr

85 7A1, reduced cellular cholesterol content in prostate cancer cell lines by inhibiting the activation

86 Prostate cancer cell lines derived from HiMyc tumors (HM

87 to actin filaments, reduced the invasion of prostate cancer cell lines in 3D in vitro assays.

88 and extracellular metabolic profiles of four prostate cancer cell lines with varying degrees of aggre

89 d epithelial-mesenchymal transition in human prostate cancer cell lines, and stable overexpression of

90 -dependent repression of ERRgamma reprograms prostate cancer cell metabolism to favor mitochondrial a

91 antitumor activity against hormone-resistant prostate cancer cells (DU145) relative to triptorelin.

92 lium-labeled HZ220 was characterized in PC-3 prostate cancer cells (PC-3), and tumor uptake in mice w

93 -sensitized naive and enzalutamide-resistant prostate cancer cells and reduced AR and AR-V7 levels to

94 rate how RAGE-PR3 interactions between human prostate cancer cells and the bone marrow microenvironme

95 pondin 2 (an MMP-3 suppressor) expression in prostate cancer cells by upregulating microRNA-128.

96 pression of MMP-3 in stromal fibroblasts and prostate cancer cells during tumor progression, clarifyi

97 rved that macrophage-driven efferocytosis of prostate cancer cells in vitro induced the expression of

98 to bone, whereas HER2 supports the growth of prostate cancer cells once they are established at metas

99 -3 (MMP-3) was lower in CAFs but elevated in prostate cancer cells relative to their normal counterpa

100 roach provides a better understanding of how prostate cancer cells respond heterogeneously to androge

101 nted here comprised either melanoma cells or prostate cancer cells stably adorned with Toll-like rece

102 inase A (AURKA) is regulated by androgens in prostate cancer cells that express high levels of AR.

103 ression of AURKA is regulated by androgen in prostate cancer cells that highly express AR, emphasizin

104 that RAGE-PR3 interaction mediates homing of prostate cancer cells to the bone marrow.

105 transcriptome profiling of 144 single LNCaP prostate cancer cells treated or untreated with androgen

106 r suspension, induced a phenotypic switch in prostate cancer cells via mechanotransduction.

107 notransduction-mediated phenotypic switch in prostate cancer cells was accompanied by decreased sensi

108 a, 4T1 mouse breast cancer, and DU 145 human prostate cancer cells were used as clinical models.

109 erformed in vitro revealed that treatment of prostate cancer cells with 27-hydroxycholesterol (27HC),

110 Treatment of CAFs but not prostate cancer cells with hydrogen peroxide directly in

111 cterized the plasticity and heterogeneity of prostate cancer cells with regard to androgen dependence

112 s red blood cells, white blood cells, DU-145 prostate cancer cells, MCF-7 breast cancer cells, and LU

113 l domain to sequester AR in the cytoplasm of prostate cancer cells, thereby reducing AR transcription

114 EAF2 in androgen regulation of DNA repair in prostate cancer cells.

115 f multiple AR-positive, but not AR-negative, prostate cancer cells.

116 en protection of DNA damage via Ku70/Ku80 in prostate cancer cells.

117 ERK pathway to promote NE differentiation of prostate cancer cells.

118 transduction-induced phenotypic switching of prostate cancer cells.

119 sion, proliferation, and malignant growth of prostate cancer cells.

120 In approximately 50% of prostate cancers, chromosomal rearrangements cause the f

121 nmet need in metastatic castration-resistant prostate cancer clinical research and practice.

122 ir diagnostic and prognostic power in future prostate cancer clinical trials.

123 cquired resistance termed castrate-resistant prostate cancer (CRPC) develops.

124 r either in the form of castration-resistant prostate cancer (CRPC) or transdifferentiated neuroendoc

125 Castration-resistant prostate cancer (CRPC) remains a major clinical challeng

126 nd progresses to lethal castration-resistant prostate cancer (CRPC).

127 tamide in patients with castration-resistant prostate cancer (CRPC).

128 ne for the treatment of castration-resistant prostate cancer (CRPC).

129 Overall, our data show that prostate cancer-derived LO powerfully promote establishm

130 nsitivity (93%) was preserved for aggressive prostate cancer detection.

131 T MR-guided biopsy is safe and effective for prostate cancer diagnosis when stratified according to P

132 ntly discovered a new molecular mechanism of prostate cancer docetaxel chemoresistance mediated by th

133 In this cohort of men with localized prostate cancer, each treatment strategy was associated

134 e evolution of therapy-induced resistance of prostate cancer either in the form of castration-resista

135 Systemic Therapy for Advanced or Metastatic Prostate Cancer: Evaluation of Drug Efficacy is a random

136 romotes tumorigenesis in the early stages of prostate cancer evolution.

137 In the retrospective cohort, luminal B prostate cancers exhibited the poorest clinical prognose

138 (European Randomized Study of Screening for Prostate Cancer) found that screening reduced prostate c

139 w AR coregulator with a multifaceted role in prostate cancer, functioning as an enhancer of the oncog

140 Men with low-risk, localised prostate cancer (Gleason pattern 3) who had received no

141 we demonstrated that although CAFs promoted prostate cancer growth, matrix metalloproteinase-3 (MMP-

142 egion-miR-383-is frequently downregulated in prostate cancer, has a critical role in determining tumo

143 oprotein convertase that is overexpressed in prostate cancer, has been shown to block cancer progress

144 vel tissue-preserving treatment for low-risk prostate cancer, has shown favourable safety and efficac

145 14; 95% CI, 1.01 to 1.29) but not high-grade prostate cancer (HR, 0.83; 95% CI, 0.64 to 1.07).

146 cancer (HR, 1.47; 95% CI, 1.13-1.92) or with prostate cancer (HR, 1.87; 95% CI, 1.14-3.06) but not fo

147 imaging helped detect clinically significant prostate cancer in 138 men.

148 on was consistently observed in the advanced prostate cancer in 18 available clinical data sets with

149 MP MR imaging depicted clinically important prostate cancer in 99 of 100 patients.

150 lysis of the RTK/ERK pathway with aggressive prostate cancer in a cohort comprising 956 aggressive an

151 e, active surveillance, in men with low-risk prostate cancer in a phase 3 trial.

152 Accurate identification of prostate cancer in frozen sections at the time of surger

153 inhibitor, decreased development of invasive prostate cancer in Pten single KO mice.

154 ucidate the tumor-suppressor role of SPOP in prostate cancer in which it acts as a negative regulator

155 nt-reported function on the 26-item Expanded Prostate Cancer Index Composite (EPIC) 36 months after e

156 es ahead of the epithelial gene signature as prostate cancer initiates and progresses.

157 During prostate cancer initiation, Nkx3.1 expression is frequen

158 Treatment of aggressive prostate cancer involves a regiment of radical prostecto

159 308) alone or combined with radiotherapy in prostate cancer IS (80.8%, n = 517).

160 ty of androgen receptor (AR) coregulators in prostate cancer is an important mechanism driving diseas

161 The course of prostate cancer is highly variable, and timely and accur

162 volved in the development and progression of prostate cancer is modeled as a combinatorial circuit.

163 adjuvant radiotherapy (aRT) in patients with prostate cancer is still limited in the United States.

164 Prostate cancer is the most common cancer diagnosis made

165 Prostate cancer is the second leading cause of cancer de

166 The first evidence of prostate cancer lesion visualization in men using (68)Ga

167 pre-, intra-, and postoperative detection of prostate cancer lesions and have high potential for futu

168 supported by the successful visualization of prostate cancer lesions in men using (68)Ga-NeoBOMB1 and

169 gression; identify mouse models for studying prostate cancer lineage plasticity; and suggest an epige

170 is limited due to difficulty of sampling as prostate cancer mainly metastasizes to bone.

171 inflammation, and expression of acknowledged prostate cancer markers.

172 ave advanced metastatic castration-resistant prostate cancer (mCRPC) and are receiving (223)RaCl2 We

173 atients with metastatic castration-resistant prostate cancer (mCRPC), overall survival (OS) is signif

174 m to anti-AR therapy in castration-resistant prostate cancer (mCRPC).

175 atients with metastatic castration-resistant prostate cancer (mCRPC).

176 injection in 203 lesions characteristic for prostate cancer (median, 10.78 vs. 12.86, P < 0.001, Wil

177 umor-initiating potential and is involved in prostate cancer metastasis via direct regulation of CD44

178 rved in circulating tumor cells (CTC) during prostate cancer metastasis.

179 is demonstrated that miR-194 is a driver of prostate cancer metastasis.

180 g allows detection of clinically significant prostate cancer missed by transrectal US-guided biopsy.

181 Purpose To characterize clinically important prostate cancers missed at multiparametric (MP) magnetic

182 The LREX' prostate cancer model is resistant to the antiandrogen e

183 , GRHL2 maintained AR expression in multiple prostate cancer model systems, was required for cell pro

184 nd BMP receptor II (BMPR2) using a Pten-null prostate cancer model.

185 We use in vitro and in vivo human prostate cancer models to show that these tumors can dev

186 in vitro and in vivo against APN-expressing prostate cancer models.

187 rostate Cancer) found that screening reduced prostate cancer mortality, but the PLCO (Prostate, Lung,

188 ciated with significantly lower all-cause or prostate-cancer mortality than observation.

189 By focusing on the neuroendocrine prostate cancer mutational data, we found prevalent ampl

190 Neuroendocrine prostate cancer (NEPC) has increasingly become a clinica

191 (CRPC) or transdifferentiated neuroendocrine prostate cancer (NEPC).

192 g indicates that mouse tumors resemble human prostate cancer neuroendocrine variants; both mouse and

193 -FER was also overexpressed in PC3 or DU145 (prostate cancer), NIH3T3 (fibroblast), H23 (lung cancer)

194 For the detection of clinically significant prostate cancer, no difference was found in the diagnost

195 In 14 prostate cancers, none had sst2 binding with the agonist

196 Purpose Men with localized prostate cancer often are treated with external radiothe

197 rent institutions assessed the likelihood of prostate cancer on a five-point scale.

198 EM135-CCDC67 and MAN2A1-FER fusions in human prostate cancer or hepatocellular carcinoma cells in vit

199 ERG is an effector of SPOP mutation in human prostate cancer or mouse models.

200 ferred approach for men with less-aggressive prostate cancer, particularly those with a prostate-spec

201 ND2 expression levels in a collection of 119 prostate cancer patient samples.

202 In 147 prostate cancer patients (mean age, 68 y; range, 44-87 y

203 circulating EV from the plasma of metastatic prostate cancer patients and was LO specific.

204 ver the mechanisms driving cell migration in prostate cancer patients are not fully understood.

205 ope-mapping of autoantibodies (AutoAbs) from prostate cancer patients identified the 78-kDa glucose-r

206 ved on pre-treatment T2-weighted MRI between prostate cancer patients who do (BCR (+)) and do not (BC

207 ameters in surgically treated, node-positive prostate cancer patients with (ENE+) vs. without (ENE-)

208 gen-receptor splice variant 7 in a cohort of prostate cancer patients with an overall concordance of

209 PET/CT affects the implemented management of prostate cancer patients with biochemical recurrence (BC

210 and cfDNA obtained from castration-resistant prostate cancer patients.

211 metastasis and for skeletal complications in prostate cancer patients.

212 A-positive lesions were detected in 12 of 12 prostate cancer patients.

213 Slow-growing prostate cancer (PC) can be aggressive in a subset of ca

214 Prostate cancer (PC) is an important medical and socio-e

215 has gained significant interest for staging prostate cancer (PC).

216 n advanced method for the staging of primary prostate cancer (PCa) and diagnosis of recurrent or meta

217 ial for the development of hormone-dependent prostate cancer (PCa) and its activity can be blocked by

218 prostate-specific membrane antigen (PSMA), a prostate cancer (PCa) biomarker, expressed on prostate t

219 lated in the arterial circulation with human prostate cancer (PCa) cells expressing IL-1beta.

220 androgen-dependent and androgen-independent prostate cancer (PCa) cells, whereas CLK2 and PAGE4 are

221 er cardiovascular (CV) risk in patients with prostate cancer (PCa) differs between those who receive

222 is-directed therapy (MDT) for oligorecurrent prostate cancer (PCa) improves progression-free survival

223 is widely used in the treatment of advanced prostate cancer (PCa) in many countries, but its effect

224 Prostate cancer (PCa) is a common cancer in men.

225 Prostate cancer (PCa) is one of the leading cancers in m

226 T/CT with (68)Ga-PSMA-11 in the diagnosis of prostate cancer (PCa) is routinely performed at 1 h afte

227 Prostate cancer (PCa) is the most common cancer in men w

228 Genetic alterations associated with prostate cancer (PCa) may be identified by sequencing me

229 ss the ability of (64)CuCl2 PET/CT to detect prostate cancer (PCa) recurrence in patients with bioche

230 Target volume delineations for prostate cancer (PCa) salvage radiotherapy (SRT) after r

231 The androgen receptor (AR) is required for prostate cancer (PCa) survival and progression, and abla

232 unctional role, and mechanisms of actions in prostate cancer (PCa)-the most common cancer type in mal

233 e current approaches to inhibit AR action in prostate cancer (PCa).

234 ed radiotherapy in high-risk, organ-confined prostate cancer (PCa).

235 idelines are limited for genetic testing for prostate cancer (PCA).

236 expressed in several human tumors, including prostate cancer (PCa).

237 n and progression of many cancers, including prostate cancer (PCa).

238 dications in recurrent as well as in primary prostate cancer, preliminary data demonstrate a substant

239 atients with metastatic castration-resistant prostate cancer previously treated with docetaxel.

240 protein thioredoxin-1 (TRX1) increases with prostate cancer progression and in androgen-deprived CRP

241 3 as a pivotal regulator of AR signaling and prostate cancer progression and suggest a functional int

242 roenvironment mediate bone metastasis during prostate cancer progression, with potential implications

243 ERK signaling pathway has been implicated in prostate cancer progression.

244 tablishing its promoting role in BMP6-driven prostate cancer progression.

245 drenergic signaling promote angiogenesis and prostate cancer progression.

246 hes for offsetting the effects of obesity on prostate cancer progression.

247 ssociated GRP78, TF expression/activity, and prostate cancer progression.

248 ndings uncover genetic mutations that enable prostate cancer progression; identify mouse models for s

249 ection of Mobilan into primary tumors of the prostate cancer-prone transgenic adenocarcinoma of the m

250 Filling this gap, we demonstrate that in prostate cancer, PSMA initiates signaling upstream of PI

251 In this cohort of men with localized prostate cancer, radical prostatectomy was associated wi

252 For patients with high-risk prostate cancer receiving EBRT and androgen-deprivation

253 Cross-sectional study in the National Prostate Cancer Register (NPCR) of Sweden from 2009 thro

254 a nested case-control study in the National Prostate Cancer Register of Sweden, which includes all 3

255 In prostate cancer, resistance to the antiandrogen enzaluta

256 can improve outcomes in men with metastatic prostate cancer resistant to traditional hormonal therap

257 ssociation was found between TRT and overall prostate cancer risk (odds ratio [OR], 1.03; 95% CI, 0.9

258 Vitamin E increased prostate cancer risk in the Selenium and Vitamin E Cance

259 o testosterone replacement therapy (TRT) and prostate cancer risk is controversial.

260 ing ligands proposed for targeted therapy of prostate cancer, RPS-027 has tumor-to-tissue ratios that

261 use of active surveillance is important for prostate cancer screening to be cost-effective.

262 vitro Here we show that in a mouse model of prostate cancer, SIN3B provides a barrier to malignant p

263 istant metastasis-free survival [DMFS], 53%; prostate cancer-specific survival [PCSS], 78%; overall s

264 s, biochemical recurrence, overall survival, prostate cancer-specific survival, associations with bio

265 In human prostate cancer specimens, EAF2 expression was inversely

266 PPARD was downregulated in prostate cancer specimens.

267 ment at 7p14.3 may predispose to SPOP mutant prostate cancer subclass through a hormone dependent DNA

268 years of follow-up among men with localized prostate cancer, surgery was not associated with signifi

269 ality of life using the validated instrument Prostate Cancer Symptom Indices was assessed at baseline

270 ome expressed in approximately 5% of primary prostate cancer that is characterized by abbreviated res

271 Prostate cancer that progresses after enzalutamide treat

272 NTEGRATE-Neo, by identifying gene fusions in prostate cancers that may produce neoantigens.

273 In prostate cancer, the development of castration resistanc

274 In prostate cancer, the gene encoding the transcription fac

275 ce of tumor suppressive activity of PPARD in prostate cancer through a noncanonical and ligand-indepe

276 ptor (AR) is critical for the progression of prostate cancer to a castration-resistant (CRPC) state.

277 r need for a molecular subtyping approach in prostate cancer to identify clinically distinct subgroup

278 we randomly assigned 731 men with localized prostate cancer to radical prostatectomy or observation.

279 atients with metastatic castration-resistant prostate cancer treated with this combination, compared

280 ing PRMT5 may represent a novel approach for prostate cancer treatment by eliminating AR expression.

281 ects of contemporary approaches to localized prostate cancer treatment could inform shared decision m

282 gene delivery approach for the treatment of prostate cancer tumors, and possibly other carcinomas wh

283 at the GR locus, but is restored in advanced prostate cancers upon reversion of both repressive signa

284 in serum samples obtained from patients with prostate cancer using both the aptasensor and Immunoradi

285 cific-related gene (ERG), or TMPRSS2:ERG, in prostate cancer varies by race.

286 Loss of CYP27A1 in prostate cancer was confirmed at the protein level by im

287 and women in SEER (lung, colon, breast, and prostate cancers), we found no significant increase in t

288 omics in a mouse model and human biopsies of prostate cancer, we identify alterations in tumours affe

289 atients with metastatic castration-resistant prostate cancer were treated with placebo alone.

290 Pooled nongastrointestinal and prostate cancers were not associated with gallstone dise

291 Recommendations For patients with low-risk prostate cancer who require or choose active treatment,

292 th high-risk, locally advanced or metastatic prostate cancer who were initiating long-term hormone th

293 robust sensitivity for detecting aggressive prostate cancer with consequent potential health care co

294 n (PSA) level, or (c) had a prior history of prostate cancer with increasing PSA level.

295 ds have shown promise for in vivo imaging of prostate cancer with PET.

296 in men with metastatic castration-resistant prostate cancer with the addition of custirsen to cabazi

297 ne the association of ADT as a treatment for prostate cancer with the subsequent development of demen

298 11-2012 with clinical stage cT1-2, localized prostate cancer, with prostate-specific antigen levels l

299 herapy-naive metastatic castration-resistant prostate cancer without visceral metastases.

300 increasingly accepted for managing low-risk prostate cancer, yet there is no consensus about impleme