ライフサイエンスコーパス: prostate cancer

1 covery rate < 0.05) (for example, NKX3-1 for prostate cancer).

2 9.7 vs. 2.3 +/- 2.6, P < 0.001, for primary prostate cancer).

3 esult in overtreatment and undertreatment of prostate cancer.

4 nimally invasive method for the diagnosis of prostate cancer.

5 re prevalent malignancies such as breast and prostate cancer.

6 ol tissue from Chinese patients with primary prostate cancer.

7 s still a mainstay of treatment for advanced prostate cancer.

8 tro demonstrated critical roles for USP22 in prostate cancer.

9 e most common genomic rearrangement in human prostate cancer.

10 is efficacious in a PSMA-expressing model of prostate cancer.

11 fic membrane antigen (PSMA) is promising for prostate cancer.

12 177)Lu-PSMA-617, is used to treat metastatic prostate cancer.

13 rotein A1 (FOXA1), an invasion suppressor in prostate cancer.

14 tions for optimal use of imaging in advanced prostate cancer.

15 a potential therapeutic target in metastatic prostate cancer.

16 conitase (ACO2) activity to favor aggressive prostate cancer.

17 of liver metastases of castration-resistant prostate cancer.

18 te myeloid leukemia (AML), breast cancer and prostate cancer.

19 ion to treat metastatic castration-resistant prostate cancer.

20 tatic hormone-naive and castration-resistant prostate cancer.

21 drives NE differentiation and glycolysis of prostate cancer.

22 l phase 3 clinical trial for PET imaging for prostate cancer.

23 onary heart disease, atrial fibrillation and prostate cancer.

24 rative in the initial management of men with prostate cancer.

25 n PET/CT is a new tool for the assessment of prostate cancer.

26 tric MRI in men with biochemically recurrent prostate cancer.

27 y of solid human tumors, including localized prostate cancer.

28 that determines the effects of senescence in prostate cancer.

29 membrane antigen (PSMA)-11 PET/CT imaging of prostate cancer.

30 alid target for therapy and/or prevention of prostate cancer.

31 sform the diagnostic field in the context of prostate cancer.

32 Regucalcin (RGN), which promotes dormancy of prostate cancer.

33 PSMA), enabling targeted beta-irradiation of prostate cancer.

34 the presence of benign prostate disease and prostate cancer.

35 r outcome in metastatic castration-resistant prostate cancer.

36 mains a major challenge in treating advanced prostate cancer.

37 n unexpected effect of promoting invasion in prostate cancer.

38 arly in patients presenting for restaging of prostate cancer.

39 ADT in men with intermediate- and high-risk prostate cancer.

40 py represent the major challenge in treating prostate cancer.

41 tween cell proliferation and invasiveness in prostate cancer.

42 o link the in vitro and in vivo evolution of prostate cancer.

43 sis and subsequent oncogenic dependencies in prostate cancer.

44 to negatively regulate miR-23c expression in prostate cancer.

45 and can potentially impact the treatment of prostate cancer.

46 e on the optimal use of imaging for advanced prostate cancer.

47 modality for metastatic castration-resistant prostate cancer.

48 ntial as lead compounds for the treatment of prostate cancer.

49 with mutations associated with resistance in prostate cancer.

50 has been observed in advanced and metastatic prostate cancers.

51 (AR) is the main strategy to treat advanced prostate cancers.

52 edisposition genes than the standard method (prostate cancer: 198 vs 182; melanoma: 93 vs 74); sensit

53 ce, 19.0%; 95% CI, 9.1% to 28.9%]), and NPV (prostate cancer: 59.3% vs 25.0% [difference, 34.3%; 95%

54 15.2%; 95% CI, 3.7% to 26.7%]), specificity (prostate cancer: 64.0% vs 36.0% [difference, 28.0%; 95%

55 98 vs 182; melanoma: 93 vs 74); sensitivity (prostate cancer: 94.7% vs 87.1% [difference, 7.6%; 95% C

56 rence, 26.8%; 95% CI, 17.6% to 35.9%]), PPV (prostate cancer: 95.7% vs 91.9% [difference, 3.8%; 95% C

57 d higher sensitivity in the mendelian genes (prostate cancer: 99.7% vs 95.1% [difference, 4.6%; 95% C

58 Prostate cancer affects one in every nine men in the USA

59 ent, in patients with biochemically relapsed prostate cancer after primary local therapy.

60 rine mechanism of antiandrogen resistance in prostate cancer amenable to clinical testing using avail

61 In the patients with primary prostate cancer, an equal number of false-positive lesio

62 tigen [PSA] <=20 ng/mL, and Grade Group 1-2) prostate cancer and 619 men with unfavorable-risk (clini

63 ortfall requires a work-up in the context of prostate cancer and a multidimensional framework for con

64 men with nonmetastatic, castration-resistant prostate cancer and a rapidly rising PSA level.

65 g AR binding sites are frequently mutated in prostate cancer and can impact enhancer activity.

66 informed them about lifetime genetic risk of prostate cancer and distinguished between "normal" and "

67 ree and bound forms to enumerate the risk of prostate cancer and has found acceptance with clinicians

68 AR plays a vital role in the progression of prostate cancer and is a crucial target for therapeutic

69 atients with metastatic castration-resistant prostate cancer and liver metastases assigned to (177)Lu

70 ty in the development of advanced metastatic prostate cancer and suggests that blocking SRC-2 to enha

71 th and social care delivered to all men with prostate cancer and their families worldwide.

72 ssification using data from 54 patients with prostate cancer and was shown to accurately differentiat

73 7 breast cancer, SW480 colon cancer, and PC3 prostate cancer), and one kind of EpCAM negative cancer

74 ignaling also reveals frequently in advanced prostate cancer, and an enrichment of androgen and Wnt s

75 e results and overdiagnosis of insignificant prostate cancer, and it is not recommended for populatio

76 PI3K/mTOR pathways are often dysregulated in prostate cancer, and may lead to decreased survival, inc

77 le in promoting metastasis of breast cancer, prostate cancer, and melanoma.

78 pressed in many tumors, including breast and prostate cancer, and therefore represent an attractive t

79 tely 15%-20% of advanced treatment-resistant prostate cancers, and this may manifest clinically as tr

80 New chemical entities for the treatment of prostate cancer are thus required, and we report here th

81 Primary prostate cancers are often multifocal, having topographi

82 Other common prostate cancer associated genes such as TMPRSS2 and ERG

83 sition to smoking and prostate cancer in the Prostate Cancer Association Group to Investigate Cancer

84 ((68)Ga-PSMA-11) for biochemically recurrent prostate cancer at a tertiary medical center.

85 all, 115 patients (68.9%) were ruled to have prostate cancer based on imaging as seen on early or sta

86 Biochemically recurrent prostate cancer (BCR) is the main indication to perform

87 utrition Cohort diagnosed with nonmetastatic prostate cancer between 1992 and 2013 were followed for

88 ndrogen receptor splice variant-7 (AR-V7) in prostate cancer biology is an unresolved question.

89 th the low concentration of 10 pM as well as prostate cancer biomarker is detected, which is owing to

90 a systematic literature review of localized prostate cancer biomarker studies between January 2013 a

91 s recommendations for available tissue-based prostate cancer biomarkers geared toward patient selecti

92 e highest priority research needs across the prostate cancer biomedical research domain, Movember con

93 cted dysregulated protease activity in human prostate cancer biopsy samples, enabling disease classif

94 This represents the first prostate cancer blood test that can predict which patien

95 We identified a Notch3-MMP-3 axis in human prostate cancer bone metastases that contributes to oste

96 ed for the treatment of castration-resistant prostate cancer but was dropped in phase III clinical tr

97 ed with the risks of colorectal, breast, and prostate cancer, but evidence for other less common canc

98 ployed the system specifically for localized prostate cancer by integrating large-scale prostate canc

99 atients with metastatic castration-resistant prostate cancer can be reassured that cabazitaxel will n

100 the intrinsic features of cell-of-origin for prostate cancers can dictate their clinical behaviors.

101 Prostate cancer (CaP) relies on methylthioadenosine phos

102 ferentiating between indolent and aggressive prostate cancers (CaP) is important to decrease overtrea

103 logies, PIONEER aims to advance the field of prostate cancer care with a particular focus on improvin

104 Because only ~10% of diagnosed prostate cancer cases are aggressive, existing practice

105 find depletion of FASN expression increases prostate cancer cell adhesiveness, impairs HGF-mediated

106 e a role of HGF/MET in beta-catenin-mediated prostate cancer cell growth and progression and implicat

107 We assessed the consequences of prostate cancer cell interaction with neural cells, whic

108 Studies of the STAT3-deficient prostate cancer cell line PC-3 (PC3) along with STAT3-pr

109 ive activity in the androgen-independent PC3 prostate cancer cell line.

110 quence, 5-AzadC induced HEXIM1 expression in prostate cancer cell lines and triple negative breast ca

111 D9 subunit, is required for the viability of prostate cancer cell lines in vitro and for optimal xeno

112 ice performance was characterized using four prostate cancer cell lines, including PC-3, VCaP, DU-145

113 terization and drug testing in a panel of 20 prostate cancer cell lines.

114 l of cancer cell lines, particularly against prostate cancer cell lines.

115 nuclear entry and functions in several human prostate cancer cell lines.

116 r tumors reduces HDL-associated increases in prostate cancer cell proliferation and disease progressi

117 as a cognate inhibitor for TMPRSS2 in human prostate cancer cells and may serve as a potential facto

118 , we performed a cell tracking experiment of prostate cancer cells in a PLA device for advanced cell

119 to decrease proliferation and metastasis of prostate cancer cells in vitro and in vivo murine xenogr

120 B1 WT (SR-B1(+/+)) and SR-B1 KO (SR-B1(-/-)) prostate cancer cells in WT and apolipoprotein-AI KO (ap

121 corroborates that the lineage status of the prostate cancer cells is a determinant for its propensit

122 Indeed, Rac1-null PC3 prostate cancer cells or cancer models with low levels o

123 e gene transcription or DNA-damage repair in prostate cancer cells that co-express AR-V7 and AR-FL.

124 EK5 knockdown by RNA interference sensitizes prostate cancer cells to ionizing radiation (IR) and eto

125 cell debris allow macropinocytic breast and prostate cancer cells to proliferate, despite fatty acid

126 fferent phenotypes in a population of murine prostate cancer cells, and describes the hysteresis in t

127 Here we show, in prostate cancer cells, that LSD1 associates with FOXA1 a

128 teractions in normal prostate epithelial and prostate cancer cells.

129 resistance to genotoxic stress in aggressive prostate cancer cells.

130 PAICS is required for growth and survival of prostate cancer cells.

131 rial nucleoside diphosphate kinase (NDPK) in prostate cancer cells.

132 and causes growth retardation in a panel of prostate cancer cells.

133 tability and changing DNA repair capacity in prostate cancer cells.

134 The taxanes are important components of prostate cancer chemotherapy regimens, but their oral ad

135 The criteria of the Prostate Cancer Clinical Trials Working Group (PCWG2) in

136 We investigated the impact of PSMA PET on Prostate Cancer Clinical Trials Working Group 3 (PCWG3)

137 thods was not significantly different in the prostate cancer cohort (94.9% vs 90.6% [difference, 4.3%

138 The prostate cancer cohort included 1072 men (mean [SD] age

139 aspartate, are widely reported as reduced in prostate cancer compared to healthy tissue and are there

140 ive phenotype to lethal castration-resistant prostate cancer (CRPC) are poorly understood.

141 ly for the treatment of castration-resistant prostate cancer (CRPC) as the oral administration of the

142 y aggressive variant of castration-resistant prostate cancer (CRPC), is increasing in incidence with

143 rs as a more aggressive castration resistant prostate cancer (CRPC).

144 mper early diagnosis of castration-resistant prostate cancer (CRPC).

145 ogy to a castration-resistant neuroendocrine prostate cancer (CRPC-NE).

146 e, an unbiased computational analysis of the prostate cancer data from The Cancer Genome Atlas reveal

147 rray results from acute myeloid leukemia and prostate cancer datasets available on TCGA.

148 in the aberrant gene expression that drives prostate cancer development.

149 A total of 1,335 patients with prostate cancer diagnosed between 2009 and 2015 were enr

150 0M0, PSA of 20-50 ng/mL, or Grade Group 3-5) prostate cancer diagnosed in 2011 through 2012, accrued

151 The genomics of primary prostate cancer differ from those of metastatic castrati

152 mone receptor and the primary drug target in prostate cancer due to its role as a lineage survival fa

153 /MRI has a high detection rate for recurrent prostate cancer, even at low PSA levels no higher than 0

154 A subset of human prostate cancer exhibits increased de novo synthesis of

155 velop indicators to better stratify low-risk prostate cancer for determining which men should go on a

156 rch UK, AstraZeneca, Prostate Cancer UK, the Prostate Cancer Foundation, the Experimental Cancer Medi

157 d then differentiating lesions suggestive of prostate cancer from those that were benign, on the basi

158 the evolutionary histories of 293 localized prostate cancers from single samples, and eighteen pipel

159 ate that elevated MYC in a subset of primary prostate cancers functions in a negative role in regulat

160 -based rare variant tests implicated a known prostate cancer gene (HOXB13), as well as a novel candid

161 ariants, we conducted an integrated study of prostate cancer genetic etiology in two cohorts using cu

162 d prostate cancer by integrating large-scale prostate cancer genomes and the prostate-specific epigen

163 To gain insights into the role of plectin in prostate cancer growth and metastasis, we performed prot

164 nificantly elevated in CRPC and NEPC, drives prostate cancer growth, and induces neuroendocrine pheno

165 show that CENPA overexpression is crucial to prostate cancer growth.

166 Bone Health and Bone-Targeted Therapies for Prostate Cancer guideline were clear, thorough, and base

167 Bone Health and Bone-Targeted Therapies for Prostate Cancer guideline.

168 Assessing genetic lifetime risk for prostate cancer has been proposed as a means of risk str

169 The current diagnostic pathway for prostate cancer has resulted in overdiagnosis and conseq

170 , however, associated with increased risk of prostate cancer (highest vs. lowest quintile: HR = 1.28,

171 er (P > 0.05) in local recurrence or primary prostate cancer; however, the tumor-to-bladder ratio was

172 roducing a genetic test for lifetime risk of prostate cancer in general practice on future PSA testin

173 igenin, a novel anti-inflammatory lignan, on prostate cancer in obese conditions both in vitro and in

174 in multiple other adenocarcinomas, including prostate cancer in the presence of antiandrogens.

175 etween genetic predisposition to smoking and prostate cancer in the Prostate Cancer Association Group

176 owel, sexual, and hormonal function-Expanded Prostate Cancer Index Composite short-form 26 domain sco

177 Advanced prostate cancer initially responds to hormonal treatment

178 Prostate cancer is a heterogeneous cancer with widely va

179 Prostate cancer is a major cause of cancer morbidity and

180 AR-independent treatment-resistant prostate cancer is a major unresolved clinical problem.

181 The treatment landscape of advanced prostate cancer is changing rapidly.

182 tion in other diseases, however, its role in prostate cancer is not definitive.

183 Prostate cancer is the second most common cancer in men

184 Conclusion: PSMA PET/CT localized prostate cancer lesions in 75% of patients and M1 diseas

185 a standard definitive treatment of localized prostate cancer (LPCa).

186 Among men with early-stage prostate cancer managed with active surveillance, a beha

187 acterized in metastatic castration-resistant prostate cancer (mCRPC) but the plasma methylome has not

188 rom those of metastatic castration-resistant prostate cancer (mCRPC).

189 options for metastatic castration-resistant prostate cancer (mCRPC).

190 c accuracy of (68)Ga-PSMA-11 PET for osseous prostate cancer metastases and improve bone uptake inter

191 Prostate cancer metastases primarily localize in the bon

192 nimal model, TMPRSS2 overexpression promoted prostate cancer metastasis, and HAI-2 overexpression eff

193 In around 20% of men with prostate cancer, metastasis develops during the course o

194 deficient mouse (Pten(Delta/Delta) BRF1(Tg)) prostate cancer model accelerated prostate carcinogenesi

195 reated a series of ATM-deficient preclinical prostate cancer models and tested the impact of ATM loss

196 Three-dimensional (3D) printed prostate cancer models are an emerging adjunct for urolo

197 ress following nutrient deprivation in three prostate cancer models displaying varying degrees of tum

198 nsitive transcriptome and ubiquitylome using prostate cancer models of clinical relevance.

199 ion of Nuclear Medicine (EANM) criteria, the Prostate Cancer Molecular Imaging Standardized Evaluatio

200 ic and epigenetic signatures associated with prostate cancer molecular subtypes, supporting the devel

201 In this study, the prostate cancer multistage murine model TRAMP and TRAMP-

202 gen receptor (AR)-independent neuroendocrine prostate cancer (NEPC) after androgen-deprivation therap

203 Neuroendocrine prostate cancer (NEPC) is an aggressive malignancy with

204 ial or complete small cell or neuroendocrine prostate cancer (NEPC) phenotype.

205 Therapy-induced neuroendocrine prostate cancer (NEPC), an extremely aggressive variant

206 lineage plasticity dynamics, exemplified by prostate cancer, NSCLC, and SCLC.

207 d of methylation patterns specific to either prostate cancer or prostate normal epithelium.

208 ith the risk of lung, breast, colorectal, or prostate cancers (OR range 0.78-1.10; P >= 0.27 for >= 2

209 Analysis of 130 prostate cancer patient serum samples revealed that some

210 Methods: Fifty-six prostate cancer patients (18 before prostatectomy and 38

211 h detection rates in biochemically recurrent prostate cancer patients and is positive in about 50% of

212 The major cause of death in prostate cancer patients can be attributed to metastatic

213 ET/CT for primary staging of treatment-naive prostate cancer patients is still under debate.

214 , current guidelines for bone assessments in prostate cancer patients should be revisited because (68

215 ctive monocentric study was conducted on 135 prostate cancer patients with biochemical recurrence and

216 Nevertheless, the majority of advanced-stage prostate cancer patients, including those with SPINK1-po

217 or cell-free DNA, isolated from the blood of prostate cancer patients, on non-tumor prostate cell lin

218 ptomic data from in vitro experiments and in prostate cancer patients, we found that a significant nu

219 study longitudinal blood plasma samples from prostate cancer patients, where longitudinal tissue biop

220 treatment in metastatic castration-resistant prostate cancer patients.

221 terns and sentinel nodes (SNs) of individual prostate cancer patients.

222 gents for (212)Pb-based TRT of patients with prostate cancer (PC) by evaluating the matching gamma-em

223 Prostate cancer (PC) care is rapidly evolving, with impr

224 7 PET for primary N-staging of patients with prostate cancer (PC) compared with morphologic imaging (

225 or microenvironment plays a critical role in prostate cancer (PC) development and progression.

226 Prostate cancer (PC) is the most frequently diagnosed ca

227 T/CT and (18)F-PSMA-1007 PET/CT in recurrent prostate cancer (PC) patients.

228 g RNT with immunotherapy in a mouse model of prostate cancer (PC).

229 atients with biochemical recurrence (BCR) of prostate cancer (PC).

230 ing men with clinically localized, high-risk prostate cancer (PC).

231 -7 PET/CT in biochemical recurrence (BCR) of prostate cancer (PCa) after radical prostatectomy (RP) u

232 nce multiparametric MRI in the prediction of prostate cancer (PCa) aggressiveness, defined by Gleason

233 O) is the main bioenergetic pathway in human prostate cancer (PCa) and a promising novel therapeutic

234 fic diagnostic and prognostic biomarkers for prostate cancer (PCa) are urgently needed.

235 Epigenetic processes govern prostate cancer (PCa) biology, as evidenced by the depen

236 Prostate cancer (PCa) cells heavily rely on an active an

237 Prostate cancer (PCa) cells were identified to secrete g

238 A monoclonal antibodies (mAbs) to assess the prostate cancer (PCa) diagnostic utility of different PS

239 Prostate cancer (PCa) is one of the most common cancers

240 Prostate cancer (PCa) is the second leading cause of can

241 brane antigen (PSMA) PET/CT on management of prostate cancer (PCa) patients with biochemical recurren

242 ermline testing (GT) is a central feature of prostate cancer (PCA) treatment, management, and heredit

243 drogen receptor (AR) action is a hallmark of prostate cancer (PCa) with androgen deprivation being st

244 dioligand therapy (RLT) is effective against prostate cancer (PCa), but all patients relapse eventual

245 to improve diagnosis and characterization of prostate cancer (PCa), but validation with histopatholog

246 response in many types of cancer, including prostate cancer (PCa), is limited.

247 active treatment for biochemically recurrent prostate cancer (PCa), whereby cycling treatment on and

248 st frequently mutated/deleted genes in human prostate cancer (PCa).

249 etection of bone metastases in patients with prostate cancer (PCa).

250 y (ADT) and radiotherapy (RT) on outcomes in prostate cancer (PCa).

251 are promising small molecules for targeting prostate cancer (PCa).

252 monitor treatment response in patients with prostate cancer (PCa).

253 iated with NE differentiation and aggressive prostate cancer phenotype.

254 tastasis, we performed proteomic analysis of prostate cancer plectin knock-down xenograft tissues.

255 base excision repair (BER) is increased with prostate cancer progression and correlates with poor pro

256 ole of KDM5B in epigenetic dysregulation and prostate cancer progression in cultured cells and in mou

257 In models of prostate cancer progression, BOP1 expression showed expr

258 lipid content and severely repressed in vivo prostate cancer progression.

259 ion did not significantly reduce the risk of prostate cancer progression.

260 In particular, we showed that, in prostate cancer, PTEN loss appears to establish an immun

261 ology and End Results Program sites and a US prostate cancer registry, with surveys through September

262 er care with a particular focus on improving prostate-cancer-related outcomes, health system efficien

263 ne checkpoint inhibition in the treatment of prostate cancer remains unclear.

264 Prostate cancer represents one of the most common forms

265 Advanced prostate cancers resistant to androgen receptor antagoni

266 simultaneously targeting this dependency in prostate cancer results in an effective therapeutic appr

267 Since HOXB13 p.G84E is a prostate cancer risk allele, we evaluated the associatio

268 Approaches to prostate cancer screening, diagnosis, surveillance, trea

269 Lethal metastatic prostate cancer seems to arise from a single clone in th

270 The mechanisms by which prostate cancer shifts from an indolent castration-sensi

271 ugh screening by serum PSA levels can reduce prostate cancer-specific mortality, it is unclear whethe

272 Immunohistochemistry analysis in human prostate cancer specimens showed that the expression of

273 mone-independent growth of breast cancer and prostate cancer spheroids and restored lumen filling in

274 In prostate cancer, SPOP seems to function as a tumour supp

275 aging is becoming the reference standard for prostate cancer staging, especially in advanced disease.

276 garding the well-known health disparities in prostate cancer, such as the higher mortality in African

277 To identify rare variants associated with prostate cancer susceptibility and better characterize t

278 progressing metastatic castration-resistant prostate cancer taken prior to starting a standard-of-ca

279 esis genes including ACLY, ACC1, and FASN in prostate cancer TCGA dataset.

280 lly engineered mouse model for non-AR-driven prostate cancer that centers on a negative regulator of

281 g overall survival of patients with advanced prostate cancer that is incurable by surgery or radiatio

282 uencing to analyze the genomic signatures of prostate cancer that progressed after targeted alpha-the

283 In men with localized prostate cancer, the addition of androgen-deprivation th

284 In prostate cancer, the AR cistrome is reprogrammed relativ

285 nique an important role in the management of prostate cancer, the most prevalent non-cutaneous cancer

286 men with nonmetastatic, castration-resistant prostate cancer, the percentage of patients who were ali

287 d mRNA were substantially decreased in human prostate cancer tissues, which positively correlated wit

288 anscript levels correlate with each other in prostate cancer tissues.

289 owever, genetic evidence in mouse models for prostate cancer to support the crucial role of Sox2 is m

290 Androgen deprivation is the cornerstone of prostate cancer treatment.

291 We conclude that knocking out SR-B1 in prostate cancer tumors reduces HDL-associated increases

292 Cancer Research UK, AstraZeneca, Prostate Cancer UK, the Prostate Cancer Foundation, the

293 over interplay in data from 67 patients with prostate cancer undergoing intermittent androgen depriva

294 ulate platform for the targeted treatment of prostate cancer using sonodynamic therapy (SDT).

295 ddition, a polygenic risk score (PRS) of 188 prostate cancer variants was strongly associated with ri

296 From these efforts, 17 research needs in prostate cancer were agreed on and prioritized, and 3 re

297 Polygenic risk scores for prostate cancer were higher in Nigeria than in Senegal.

298 potential to alter clinical outcome in human prostate cancer, where low levels of C7 associate with p

299 ong men with metastatic castration-resistant prostate cancer who had tumors with at least one alterat

300 a of the European Association of Urology and Prostate Cancer Working Group 3.