ライフサイエンスコーパス: bone metastasis

1 ceived MF-tricyclic after the development of bone metastasis).

2 ease bone stromal activity in the absence of bone metastasis.

3 and pathophysiology to models of prostate-to-bone metastasis.

4 variables were significantly associated with bone metastasis.

5 mph node, and 15.9% (11 patients) a solitary bone metastasis.

6 erapeutic targets and clinical biomarkers of bone metastasis.

7 the SK3 channel was markedly associated with bone metastasis.

8 ays was associated with an increased risk of bone metastasis.

9 e cancer cells and osteoclasts might promote bone metastasis.

10 s osteoclast activity and reduces osteolytic bone metastasis.

11 or Enpp1 in the development of breast cancer bone metastasis.

12 ncer (MTC) patient's risk of lung, liver, or bone metastasis.

13 iver metastasis, and 34 patients (4.8%) with bone metastasis.

14 ates osteoclastogenesis during breast cancer bone metastasis.

15 y to therapeutically influence breast cancer bone metastasis.

16 ventive protocol with halofuginone inhibited bone metastasis.

17 und that reduction of OGT expression blocked bone metastasis.

18 specimens from patients with lymph node and bone metastasis.

19 d hepatic cancers, as well as the process of bone metastasis.

20 vitro and in a mouse model of human melanoma bone metastasis.

21 osteolytic cycle in this MDA-MB-231 model of bone metastasis.

22 nically for the treatment of prostate cancer bone metastasis.

23 r high risks of lung metastasis, but not for bone metastasis.

24 n osteoblast-cancer cell interactions and in bone metastasis.

25 and lung metastasis but is nonessential for bone metastasis.

26 al cells and are of paramount importance for bone metastasis.

27 may stand as a novel mechanism for promoting bone metastasis.

28 tential therapeutic target for breast cancer bone metastasis.

29 ain cancer and for the palliation of pain in bone metastasis.

30 d osteoclast function and are protected from bone metastasis.

31 vironment in favor of osteoclastogenesis and bone metastasis.

32 lpha (IL-11Ralpha) is a functional target in bone metastasis.

33 stromal interactions that promote osteolytic bone metastasis.

34 egulation of biological activity of SPARC in bone metastasis.

35 he consequences of this osteoclast defect in bone metastasis.

36 its disruption leads to a decrease in tumor bone metastasis.

37 th castration-resistant prostate cancer with bone metastasis.

38 tic target in the treatment of breast cancer bone metastasis.

39 e progression and treatment of breast cancer bone metastasis.

40 XCR4 in osteoclastogenesis and in a model of bone metastasis.

41 egulation of VEGF and may pre-dispose to PCa bone metastasis.

42 apies for osteopenic bone defects and cancer bone metastasis.

43 oclastic bone resorption and prostate cancer bone metastasis.

44 -human model of experimental prostate cancer bone metastasis.

45 -human model of experimental prostate cancer bone metastasis.

46 for the treatment of lethal prostate cancer bone metastasis.

47 o is a candidate mediator of prostate cancer bone metastasis.

48 bone resorption characteristic of osteolytic bone metastasis.

49 rostate cancer cell line with propensity for bone metastasis.

50 ng drug for the treatment of prostate cancer bone metastasis.

51 astatic, in the development of breast cancer bone metastasis.

52 cluding an in vivo model for prostate cancer bone metastasis.

53 ndependently predicted shorter time to first bone metastasis.

54 roved to be nonosseous or false-positive for bone metastasis.

55 den and bone degradation in animal models of bone metastasis.

56 ntake in oncology outpatients with pain from bone metastasis.

57 en increasingly used in treatment of painful bone metastasis.

58 ll mitogen and promoter of osteolysis during bone metastasis.

59 uppresses experimental human prostate cancer bone metastasis.

60 cal approach for diagnosis and assessment of bone metastasis.

61 unity to improve therapeutic intervention of bone metastasis.

62 Targeting S100A4 and GRM3 may help prevent bone metastasis.

63 line, RBM1-IT4, established from a human RCC bone metastasis.

64 increased Gleason score, advanced stage and bone metastasis.

65 into the capacity of these drugs to prevent bone metastasis.

66 malignancy (HHM) that occurs with or without bone metastasis.

67 asing skeletal tumor burden in patients with bone metastasis.

68 state cancer xenograft tissue derived from a bone metastasis.

69 ases in a well-characterized animal model of bone metastasis.

70 tic agent for the prevention or treatment of bone metastasis.

71 vel therapeutic target for breast cancer and bone metastasis.

72 echanisms contributing to the early steps of bone metastasis.

73 t anionic PTX-NPs, slowed the progression of bone metastasis.

74 n and TGFbeta-induced osteoclastogenesis for bone metastasis.

75 teocytes in the suppression of breast cancer bone metastasis.

76 aling-mediated bFGF in the bone promotes BCa bone metastasis.

77 on breast cancer cell growth, migration and bone metastasis.

78 on of TWIST1, thereby leading to accelerated bone metastasis.

79 ism accounting for the TGFbeta signaling and bone metastasis.

80 activate PTHrP and promote TGF-beta-induced bone metastasis.

81 rvival of patients with prostate cancer with bone metastasis.

82 ly extended survival of mice with MDA-MB-231 bone metastasis.

83 r, as a factor that promotes prostate cancer bone metastasis.

84 , and both were equally excellent for pelvic bone metastasis.

85 grin is upregulated in human prostate cancer bone metastasis.

86 n mice, while DLC1 overexpression suppressed bone metastasis.

87 plicate Rho-TGF-beta crosstalk in osteolytic bone metastasis.

88 ne marrow for the treatment of breast cancer bone metastasis.

89 strategies against primary bone tumours and bone metastasis.

90 how the TGF-beta pathway is regulated during bone metastasis.

91 xpression exhibited enhanced capabilities of bone metastasis.

92 mab also significantly delayed time to first bone metastasis (33.2 [95% CI 29.5-38.0] vs 29.5 [22.4-3

93 e characteristics could be explored to treat bone metastasis, a significant clinical issue in prostat

94 In the mouse model of bone metastasis, A77636 reduced osteolytic lesions and p

95 se (Src) is implicated in the development of bone metastasis and castration resistance of prostate ca

96 The mechanism involved in bone metastasis and destruction in neuroblastoma is poor

97 review, we evaluate the importance of ERs in bone metastasis and discuss new avenues of investigation

98 verexpression was sufficient to reconstitute bone metastasis and ERK signaling in cells expressing hi

99 by modulating SPARC, a protein implicated in bone metastasis and inflammation.

100 osteolytic bone diseases such as osteolytic bone metastasis and inflammatory osteolysis.

101 l would inhibit experimental prostate cancer bone metastasis and preserve bone structure.

102 represent a potential therapeutic target in bone metastasis and provide a rationale for the developm

103 nt samples from men with prostate cancer and bone metastasis and showed by immunohistochemical analys

104 egarding the clinical and economic burden of bone metastasis and skeletal-related events (SREs) in pr

105 Bone metastasis and SREs in prostate cancer patients are

106 ertinent information regarding the burden of bone metastasis and SREs.

107 velocity independently predict time to first bone metastasis and survival.

108 ature that promotes osteolytic breast cancer bone metastasis and that inhibition of such interactions

109 ate bone tumor progression in a rat model of bone metastasis and that this protocol could be translat

110 referred site for breast and prostate cancer bone metastasis and the hematologic malignancy, multiple

111 el of high-penetrance spontaneous osteolytic bone metastasis and underscore the critical role of nonm

112 uld be useful for inhibiting prostate cancer bone metastasis and, as such, may enhance the therapeuti

113 rimental models, depletion of FN14 inhibited bone metastasis, and FN14 could be functionally reconsti

114 has been implicated as a critical factor in bone metastasis, and here we show that SRC is a direct t

115 IN28 depletion and let-7 expression suppress bone metastasis, and LIN28 restores bone metastasis in m

116 in detecting liver metastasis, lymph nodes, bone metastasis, and primary lesion was 95%, 95%, 90%, a

117 osteolysis in an intratibial mouse model of bone metastasis, and that soluble factor(s) shed by tumo

118 f the bone remodeling process for therapy of bone metastasis, and to determine how different cell sub

119 ermine the correlation between the volume of bone metastasis as assessed with diffusion-weighted (DW)

120 particularly in patients with lymph node or bone metastasis as compared to those with localized brea

121 lium, with highest levels observed in breast-bone metastasis as determined by qRT-PCR and immunohisto

122 hemical progression, 'progressing', and (iv) bone metastasis at presentation 'metastatic'.

123 n osteoclast differentiation, correlate with bone metastasis burden.

124 lA in the metastatic PC3 cell line inhibited bone metastasis but did not affect subcutaneous tumor gr

125 oRNAs in malignant cells suppresses lung and bone metastasis by human cancer cells in vivo.

126 ing is frequently more specific at detecting bone metastasis by measuring the accumulation of radiotr

127 interaction could contribute to preferential bone metastasis by prostate carcinoma cells.

128 enosumab also consistently increased time to bone metastasis by PSADT subset.

129 receptor (EGFR) inhibitors block osteolytic bone metastasis by targeting EGFR signaling in bone stro

130 rmation regarding the presence or absence of bone metastasis by using a five-point grading system (0,

131 To study the role of Notch3 signaling in bone metastasis, cancer cells were inoculated into athym

132 gan-confined prostate cancer and in 25 of 25 bone metastasis cases studied.

133 or the necessity for radiation or surgery to bone metastasis cause considerable morbidity, decrements

134 t a COX-2 inhibitor, MF-tricyclic, inhibited bone metastasis caused by a bone-seeking clone both in p

135 apy decreases development and progression of bone metastasis caused by melanoma cells through the inh

136 tein in the SCID-human model of experimental bone metastasis could be mediated by regulation of OPG/R

137 In the bone metastasis-derived PC-3 prostate cancer cells, BMP7

138 teoclast progenitor that specifically drives bone metastasis during cancer progression.

139 and the bone marrow microenvironment mediate bone metastasis during prostate cancer progression, with

140 otential role of Enpp1 in the development of bone metastasis, Enpp1 expression was stably increased i

141 portance of identifying molecular drivers of bone metastasis for new therapeutic targets.

142 ight offer a new possibility for diminishing bone metastasis formation.Significance: These findings e

143 ce-free interval (0.75, 0.57-0.99; p=0.045), bone metastasis-free interval (0.62, 0.40-0.95; p=0.027)

144 interval (0.62, 0.40-0.95; p=0.027), and non-bone metastasis-free interval (0.63, 0.43-0.91; p=0.014)

145 -free interval (0.83, 0.67-1.04; p=0.10), or bone metastasis-free interval (0.77, 0.55-1.07; p=0.12).

146 Non-bone metastasis-free interval was slightly increased wit

147 monoclonal antibody, significantly increases bone metastasis-free survival (BMFS; hazard ratio [HR],

148 ly and inversely correlated to brain but not bone metastasis-free survival of patients with breast ca

149 Median bone metastasis-free survival was 30 months.

150 Denosumab significantly increased bone-metastasis-free survival by a median of 4.2 months

151 The primary endpoint was bone-metastasis-free survival, a composite endpoint dete

152 Furthermore, hBMSCs alter tumor growth and bone metastasis frequency.

153 cluded at least one radiologically confirmed bone metastasis from a histologically confirmed breast c

154 ical practice for treatment of patients with bone metastasis from breast cancer.

155 hosphonate treatment for multiple myeloma or bone metastasis from breast, prostate, or lung cancer.

156 phase 3 trial in which men with at least one bone metastasis from castration-resistant prostate cance

157 77636 on bone quality using a mouse model of bone metastasis from mammary tumor.

158 lecular mechanisms governing prostate cancer bone metastasis, FVB murine prostate epithelium was tran

159 rgets (HMGA2, BACH1) that in turn upregulate bone metastasis genes (MMP1, OPN, CXCR4).

160 tastasis signature, but only activates a few bone metastasis genes, among which DUSP1 was functionall

161 The role of CD47 in skeletal homeostasis and bone metastasis has not been described.

162 lopments in animal models of prostate cancer bone metastasis have renewed interest in the traditional

163 CC-induced osteolysis is unknown, studies of bone metastasis have shown that tumor-induced changes in

164 sions and thus helping avoid misdiagnosis of bone metastasis; however, CT revealed morphologic change

165 ing physicians recorded definite findings of bone metastasis in 14%, 29%, and 76% for IS, FOM, and PO

166 eft cardiac ventricle resulted in osteolytic bone metastasis in 74% of beta3+/+ mice by 14 days.

167 Moreover, the extent of bone metastasis in a mouse intratibial model was signifi

168 -3M-Pro4Luc2 cells in zebrafish and inhibits bone metastasis in a preclinical mouse model.

169 signal-regulated kinase (ERK) signaling and bone metastasis in a xenograft model.

170 presses breast tumour cell intravasation and bone metastasis in an orthotopic murine model.

171 he TbetaRI-I can inhibit both early lung and bone metastasis in animal model systems and suggest anti

172 an breast cancer cell lines known to produce bone metastasis in animal models compared to non-metasta

173 ression is associated with increased risk of bone metastasis in breast cancer patients.

174 y gland development and the establishment of bone metastasis in breast cancer, and NRIP1 (21q21) enco

175 only tumor angiogenesis but also osteolytic bone metastasis in breast cancer.

176 trix and serves as a key factor in promoting bone metastasis in cancer.

177 R], 0.85; P = .028) and delays time to first bone metastasis in men with nonmetastatic castration-res

178 effects of zoledronic acid on time to first bone metastasis in men with prostate cancer, no bone met

179 eting of the bone microenvironment can delay bone metastasis in men with prostate cancer.

180 t allows rater-independent quantification of bone metastasis in metastatic prostate cancer.

181 suppress bone metastasis, and LIN28 restores bone metastasis in mice bearing RKIP-expressing breast t

182 various aspects of metastasis in general and bone metastasis in particular.

183 ion inversely correlated with recurrence and bone metastasis in prostate cancer patients.

184 t transcription and that miR-96 promotes the bone metastasis in prostate cancer.

185 cur in half of prostate cancer patients with bone metastasis in the absence of treatment, and 30-45%

186 is study, we illuminate pathways relevant to bone metastasis in this disease.

187 current gaps in understanding the impact of bone metastasis in this disease.

188 uced in breast cancer cells is important for bone metastasis in this model including (1) COX-2 transf

189 the induction of IL-11, a gene implicated in bone metastasis in this mouse model system.

190 y reduced PTHLH production and breast cancer bone metastasis in vitro and in vivo.

191 Reversine suppresses MCF-7 tumour growth and bone metastasis in vivo by reducing tumour stromalizatio

192 ogic sympathetic activation on breast cancer bone metastasis in vivo can be blocked with the beta-blo

193 reduced collagen I degradation in vitro and bone metastasis in vivo.

194 esulted in fewer para-aortic lymph nodes and bone metastasis in vivo.

195 d whether MAF amplification (a biomarker for bone metastasis) in primary tumours could predict the tr

196 ltivariate logistic regressions on liver and bone metastasis, in which the number of involved nodes w

197 ysis revealed several potential mediators of bone metastasis, including the pyrophosphate-generating

198 h in vivo in a SCID-hu model of experimental bone metastasis induced by C4-2b prostate cancer cells.

199 Breast to bone metastasis is a common occurrence in the majority o

200 Bone metastasis is a common sequella of solid malignant

201 Bone metastasis is a frequent complication of breast can

202 Bone metastasis is a hallmark of advanced prostate and b

203 Bone metastasis is a leading cause of morbidity and mort

204 Bone metastasis is a major health threat to breast cance

205 Bone metastasis is a prominent cause of morbidity and mo

206 omas such as breast cancer, where osteolytic bone metastasis is associated with increased morbidity a

207 omical site of breast cancer metastasis, and bone metastasis is associated with increased morbidity a

208 nt when the efficacy of radiation therapy on bone metastasis is evaluated using FDG PET after irradia

209 Prostate cancer (PCa) bone metastasis is frequently associated with bone-formi

210 l's acquisition of properties for successful bone metastasis is influenced by signals from the stroma

211 Bone metastasis is mediated by complex interactions betw

212 Bone metastasis is one of the predominant causes of canc

213 Bone metastasis is the hallmark of progressive and castr

214 Critical to our ability to prevent and treat bone metastasis is the identification of the key factors

215 Bone metastasis is the major reason for death caused by

216 Bone metastasis is the most frequent complication of pro

217 Bone metastasis is very common in advanced prostate canc

218 g of the key mechanisms involved in CaP cell bone metastasis is vital to development of novel treatme

219 Knockdown of DLC1 in cancer cells promoted bone metastasis, leading to manifested osteolysis and ac

220 We further observed that osteolytic bone metastasis led to a decrease in HA nanocrystal size

221 software tool to automatically quantify the bone metastasis load in PSMA PET/CT.

222 such differences, we established an ex vivo bone metastasis model, termed bone-in-culture array or B

223 Using an in vivo bone metastasis model, we found that constitutive NF-kap

224 Xenografts in nude mice and bone metastasis models confirmed the remarkable aggressi

225 Bone metastasis occurs as a result of a complex pathophy

226 ovariectomy-induced osteoporosis, as well as bone metastasis of breast and skin cancers, are diminish

227 us, be a yet unrecognized lipid mediator for bone metastasis of breast cancer and a new target for an

228 ctor signaling and metabolic pathways during bone metastasis of breast cancer are not clear.

229 kappaB and found that it mediates osteolytic bone metastasis of breast cancer by stimulating osteocla

230 ppaB) plays a crucial role in the osteolytic bone metastasis of breast cancer by stimulating osteocla

231 rgets for simultaneously inhibiting lung and bone metastasis of breast cancer.

232 promising therapeutic targets for inhibiting bone metastasis of breast cancer.

233 to confer skeletal protection and ameliorate bone metastasis of cancers.

234 In addition to its inhibitory effect on bone metastasis of Jagged1-expressing tumor cells, 15D11

235 ncluding (1) COX-2 transfection enhanced the bone metastasis of MDA-435S cells and (2) breast cancer

236 is one mechanism that leads to osteoblastic bone metastasis of PCa.

237 Using a cell line from bone metastasis of prostate cancer (PC3), we analyzed ho

238 blood monocytes isolated from patients with bone metastasis of prostate cancer were more efferocytic

239 Preferential bone metastasis of prostate carcinoma cells may therefor

240 Bone metastasis often emerges long after the initial dis

241 Moreover, patients with bone metastasis only had superior survival compared to o

242 RANKL monoclonal antibody, for prevention of bone metastasis or death in non-metastatic castration-re

243 To identify men at greatest risk for bone metastasis or death, we evaluated relationships bet

244 s with shorter PSADT are at greater risk for bone metastasis or death.

245 dentified for the GEP NET patients, not even bone metastasis or estimated BM dose.

246 nd platelet beta3 integrins in this model of bone metastasis, osteoclast-defective src-/- mice were u

247 agnosis ( P = .02), higher rate of liver and bone metastasis ( P </= .02), shorter relapse-free survi

248 Cumulative rates of lung, liver, and bone metastasis, plotted against the number of lymph nod

249 characterized by solid histology, liver and bone metastasis, poor prognosis, and potential responsiv

250 k factors were assessed: sex, age over 70 y, bone metastasis, prior chemotherapy, prior external-beam

251 nodeficient mouse model of extravasation and bone metastasis produced detectable, progressive osteoly

252 We further confirm the bone metastasis-promoting function of osteoblast-derived

253 on-resistant prostate cancer at high risk of bone metastasis (prostate-specific antigen [PSA] >/=8.0

254 Using a new syngeneic model of bone metastasis (r3T), we examined whether OPN-deficient

255 ER mutations, especially their enrichment in bone metastasis, raised even more provocative questions

256 steoclast stimulatory factor secreted by RCC bone metastasis (RBM).

257 significantly associated with brain but not bone metastasis regardless of TNBC status.

258 Diagnosis of bone metastasis requires a combination of multiple imagi

259 Because prostate cancer bone metastasis requires remodeling of the collagen-rich

260 the mechanism of MMP13-dependent osteolytic bone metastasis revealed that MMP13-ASO treatment decrea

261 regarding risk factors for lung, liver, and bone metastasis, risk stratification is liable to be hap

262 Metastatic prostate cancer cell lines and bone metastasis samples displayed robust fetuin-A expres

263 routine MR imaging protocol for node and/or bone metastasis screening, which included coronal two-di

264 n for prevention of osteoclastic activity of bone metastasis, secondary to breast cancer, was identif

265 om control or tumor-bearing mice that lacked bone metastasis, signifying the essential cross-talk bet

266 The tumor-associated osteoblasts in PCa bone metastasis specimens and patient-derived xenografts

267 nt determined by time to first occurrence of bone metastasis (symptomatic or asymptomatic) or death f

268 the IL-11Ralpha-targeted proapoptotic agent bone metastasis-targeting peptidomimetic (BMTP-11) in pr

269 The bone-metastasis-targeting ability of these probes is fur

270 PDX) of castration-resistant prostate cancer bone metastasis that we exploited as a model of AVPC.

271 ediated anticancer drug delivery to sites of bone metastasis, thereby inhibiting cancer progression a

272 and specific role of NF-kappaB in osteolytic bone metastasis through GM-CSF induction, suggesting tha

273 in vivo in an immunodeficient mouse model of bone metastasis through upregulation of MMP2, but not MM

274 0 was also highly expressed in breast cancer bone-metastasis tissue.

275 g tumor cells, 15D11 dramatically sensitizes bone metastasis to chemotherapy, which induces Jagged1 e

276 of breast cancer which exhibits spontaneous bone metastasis to evaluate the function and therapeutic

277 r cell line MDA PCa 2b, derived from a human bone metastasis, to generate an invasive subline (MDA-I)

278 treatment response in patients with painful bone metastasis treated with palliative RT.

279 and discuss new avenues of investigation for bone metastasis treatment based on current knowledge.

280 1alpha was detected in the hypoxic region of bone metastasis tumors in a mouse model of human melanom

281 (P < 0.0001) and also between patients with bone metastasis versus patients with soft-tissue metasta

282 nt differences in survival for patients with bone metastasis versus soft-tissue or no metastasis for

283 by cytotoxic chemotherapy can contribute to bone metastasis via a transient increase in bone marrow

284 ependent on tumor grade, and the presence of bone metastasis was associated with worse overall surviv

285 tation studies showed that susceptibility to bone metastasis was conferred by a bone marrow-derived c

286 erformed, and radioactivity deposited in the bone metastasis was determined using region-of-interest

287 the role of bisphosphonates in patients with bone metastasis was established.

288 ne expression in patients with lymph node or bone metastasis was significantly reduced as compared wi

289 In the case of bone, metastasis was to the human implant and not the mo

290 c and genotypic alterations before and after bone metastasis, we conducted genome-wide mRNA profiling

291 immunocompetent mouse model of breast cancer bone metastasis, we confirmed that MDSC isolated from th

292 mmunocompetent mouse models of breast cancer bone metastasis, we identified a key role for pDC in fac

293 Using a mouse model of bone metastasis, we provide experimental evidence that a

294 The risks of disease recurrence and bone metastasis were also significantly lower.

295 Multiple BM and the presence of liver or bone metastasis were independent adverse prognostic fact

296 re of >or= 2.5, and radiographic evidence of bone metastasis were recruited for this longitudinal stu

297 ents with renal cell carcinoma (RCC) develop bone metastasis, which is characterized by extensive ost

298 lls inhibits bone lysis associated with C4-2 bone metastasis, which results in net increases in bone

299 Bone metastasis will impact most men with advanced prost

300 n of CD97 in PC3 cells resulted in decreased bone metastasis without affecting subcutaneous tumor gro