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1 ceived MF-tricyclic after the development of bone metastasis).
2 n and TGFbeta-induced osteoclastogenesis for bone metastasis.
3 teocytes in the suppression of breast cancer bone metastasis.
4 aling-mediated bFGF in the bone promotes BCa bone metastasis.
5 on breast cancer cell growth, migration and bone metastasis.
6 on of TWIST1, thereby leading to accelerated bone metastasis.
7 ism accounting for the TGFbeta signaling and bone metastasis.
8 activate PTHrP and promote TGF-beta-induced bone metastasis.
9 rvival of patients with prostate cancer with bone metastasis.
10 ly extended survival of mice with MDA-MB-231 bone metastasis.
11 r, as a factor that promotes prostate cancer bone metastasis.
12 , and both were equally excellent for pelvic bone metastasis.
13 grin is upregulated in human prostate cancer bone metastasis.
14 n mice, while DLC1 overexpression suppressed bone metastasis.
15 plicate Rho-TGF-beta crosstalk in osteolytic bone metastasis.
16 ne marrow for the treatment of breast cancer bone metastasis.
17 strategies against primary bone tumours and bone metastasis.
18 how the TGF-beta pathway is regulated during bone metastasis.
19 xpression exhibited enhanced capabilities of bone metastasis.
20 and pathophysiology to models of prostate-to-bone metastasis.
21 variables were significantly associated with bone metastasis.
22 gery, and radiation had lower OR factors for bone metastasis.
23 mph node, and 15.9% (11 patients) a solitary bone metastasis.
24 erapeutic targets and clinical biomarkers of bone metastasis.
25 the SK3 channel was markedly associated with bone metastasis.
26 ays was associated with an increased risk of bone metastasis.
27 e cancer cells and osteoclasts might promote bone metastasis.
28 s osteoclast activity and reduces osteolytic bone metastasis.
29 or Enpp1 in the development of breast cancer bone metastasis.
30 ncer (MTC) patient's risk of lung, liver, or bone metastasis.
31 iver metastasis, and 34 patients (4.8%) with bone metastasis.
32 ates osteoclastogenesis during breast cancer bone metastasis.
33 els, and T1 and N0 stages have a high OR for bone metastasis.
34 y to therapeutically influence breast cancer bone metastasis.
35 ventive protocol with halofuginone inhibited bone metastasis.
36 und that reduction of OGT expression blocked bone metastasis.
37 specimens from patients with lymph node and bone metastasis.
38 d hepatic cancers, as well as the process of bone metastasis.
39 vitro and in a mouse model of human melanoma bone metastasis.
40 osteolytic cycle in this MDA-MB-231 model of bone metastasis.
41 nically for the treatment of prostate cancer bone metastasis.
42 r high risks of lung metastasis, but not for bone metastasis.
43 n osteoblast-cancer cell interactions and in bone metastasis.
44 and lung metastasis but is nonessential for bone metastasis.
45 al cells and are of paramount importance for bone metastasis.
46 may stand as a novel mechanism for promoting bone metastasis.
47 tential therapeutic target for breast cancer bone metastasis.
48 ain cancer and for the palliation of pain in bone metastasis.
49 d osteoclast function and are protected from bone metastasis.
50 vironment in favor of osteoclastogenesis and bone metastasis.
51 eir potential to diminish progression of PCa bone metastasis.
52 lpha (IL-11Ralpha) is a functional target in bone metastasis.
53 egulation of biological activity of SPARC in bone metastasis.
54 nd Glg1 are instrumental to the formation of bone metastasis.
55 he consequences of this osteoclast defect in bone metastasis.
56 its disruption leads to a decrease in tumor bone metastasis.
57 th castration-resistant prostate cancer with bone metastasis.
58 tic target in the treatment of breast cancer bone metastasis.
59 ecules as a potential novel route to mediate bone metastasis.
60 XCR4 in osteoclastogenesis and in a model of bone metastasis.
61 s educate OCys to promote progression of PCa bone metastasis.
62 egulation of VEGF and may pre-dispose to PCa bone metastasis.
63 apies for osteopenic bone defects and cancer bone metastasis.
64 oclastic bone resorption and prostate cancer bone metastasis.
65 -human model of experimental prostate cancer bone metastasis.
66 -human model of experimental prostate cancer bone metastasis.
67 for the treatment of lethal prostate cancer bone metastasis.
68 o is a candidate mediator of prostate cancer bone metastasis.
69 bone resorption characteristic of osteolytic bone metastasis.
70 olony formation in the bone environment, and bone metastasis.
71 rug is able to cure breast cancer-associated bone metastasis.
72 press both tumor and stromal compartments of bone metastasis.
73 ), are key mediators of prostate-cancer (PC) bone metastasis.
74 ker and suggests therapeutic targets for PCa bone metastasis.
75 ates bone loss from breast cancer-associated bone metastasis.
76 y on its role as a functional mediator of PC bone metastasis.
77 ies, and ultimately results in prevention of bone metastasis.
78 uced CXCL12 axis diminished exosome-mediated bone metastasis.
79 , and also the effects of FGFR inhibition in bone metastasis.
80 ification of mechanisms and therapeutics for bone metastasis.
81 to colonization is the rate-limiting step of bone metastasis.
82 or adjuvant therapy to prevent breast cancer bone metastasis.
83 ease bone stromal activity in the absence of bone metastasis.
84 tic agent for the prevention or treatment of bone metastasis.
85 stromal interactions that promote osteolytic bone metastasis.
86 e progression and treatment of breast cancer bone metastasis.
87 Targeting S100A4 and GRM3 may help prevent bone metastasis.
88 vel therapeutic target for breast cancer and bone metastasis.
89 echanisms contributing to the early steps of bone metastasis.
90 t anionic PTX-NPs, slowed the progression of bone metastasis.
91 mab also significantly delayed time to first bone metastasis (33.2 [95% CI 29.5-38.0] vs 29.5 [22.4-3
92 e characteristics could be explored to treat bone metastasis, a significant clinical issue in prostat
94 ancer suffer from cancer pain as a result of bone metastasis and bone destruction, but how PD-1 block
95 ul examination of current PARP inhibitors on bone metastasis and bone loss, and suggest cotreatment w
96 se (Src) is implicated in the development of bone metastasis and castration resistance of prostate ca
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
102 othelial cells or EphB4 inhibition increases bone metastasis and shortens the time window to hind-lim
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
107 ature that promotes osteolytic breast cancer bone metastasis and that inhibition of such interactions
108 ate bone tumor progression in a rat model of bone metastasis and that this protocol could be translat
109 referred site for breast and prostate cancer bone metastasis and the hematologic malignancy, multiple
110 uld be useful for inhibiting prostate cancer bone metastasis and, as such, may enhance the therapeuti
111 rimental models, depletion of FN14 inhibited bone metastasis, and FN14 could be functionally reconsti
112 has been implicated as a critical factor in bone metastasis, and here we show that SRC is a direct t
113 IN28 depletion and let-7 expression suppress bone metastasis, and LIN28 restores bone metastasis in m
114 in detecting liver metastasis, lymph nodes, bone metastasis, and primary lesion was 95%, 95%, 90%, a
115 osteolysis in an intratibial mouse model of bone metastasis, and that soluble factor(s) shed by tumo
116 f the bone remodeling process for therapy of bone metastasis, and to determine how different cell sub
118 ermine the correlation between the volume of bone metastasis as assessed with diffusion-weighted (DW)
119 lium, with highest levels observed in breast-bone metastasis as determined by qRT-PCR and immunohisto
123 lA in the metastatic PC3 cell line inhibited bone metastasis but did not affect subcutaneous tumor gr
125 hose direct binding to cancer cells promotes bone metastasis by inducing mesenchymal-epithelial trans
126 ing is frequently more specific at detecting bone metastasis by measuring the accumulation of radiotr
128 receptor (EGFR) inhibitors block osteolytic bone metastasis by targeting EGFR signaling in bone stro
130 To study the role of Notch3 signaling in bone metastasis, cancer cells were inoculated into athym
132 or the necessity for radiation or surgery to bone metastasis cause considerable morbidity, decrements
133 t a COX-2 inhibitor, MF-tricyclic, inhibited bone metastasis caused by a bone-seeking clone both in p
134 apy decreases development and progression of bone metastasis caused by melanoma cells through the inh
135 tein in the SCID-human model of experimental bone metastasis could be mediated by regulation of OPG/R
137 alysis of matched primary breast tumours and bone metastasis-derived patient-derived xenografts (PDX)
138 extremities (total-body acquisition) affects bone metastasis detection rates and patient management.
140 and the bone marrow microenvironment mediate bone metastasis during prostate cancer progression, with
141 otential role of Enpp1 in the development of bone metastasis, Enpp1 expression was stably increased i
143 hat ephrin-B2-EphB4 communication influences bone metastasis formation by altering melanoma cell repu
144 ight offer a new possibility for diminishing bone metastasis formation.Significance: These findings e
145 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)
146 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)
147 -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).
149 monoclonal antibody, significantly increases bone metastasis-free survival (BMFS; hazard ratio [HR],
150 y and locoregional treatments would increase bone metastasis-free survival in women with breast cance
151 ly and inversely correlated to brain but not bone metastasis-free survival of patients with breast ca
157 cluded at least one radiologically confirmed bone metastasis from a histologically confirmed breast c
159 hosphonate treatment for multiple myeloma or bone metastasis from breast, prostate, or lung cancer.
160 phase 3 trial in which men with at least one bone metastasis from castration-resistant prostate cance
162 lecular mechanisms governing prostate cancer bone metastasis, FVB murine prostate epithelium was tran
164 tastasis signature, but only activates a few bone metastasis genes, among which DUSP1 was functionall
166 CC-induced osteolysis is unknown, studies of bone metastasis have shown that tumor-induced changes in
168 ing physicians recorded definite findings of bone metastasis in 14%, 29%, and 76% for IS, FOM, and PO
172 Ralpha to PC-3 cells significantly increased bone metastasis in an experimental murine metastasis mod
174 he TbetaRI-I can inhibit both early lung and bone metastasis in animal model systems and suggest anti
175 an breast cancer cell lines known to produce bone metastasis in animal models compared to non-metasta
177 y gland development and the establishment of bone metastasis in breast cancer, and NRIP1 (21q21) enco
180 R], 0.85; P = .028) and delays time to first bone metastasis in men with nonmetastatic castration-res
183 suppress bone metastasis, and LIN28 restores bone metastasis in mice bearing RKIP-expressing breast t
188 cur in half of prostate cancer patients with bone metastasis in the absence of treatment, and 30-45%
191 uced in breast cancer cells is important for bone metastasis in this model including (1) COX-2 transf
193 Reversine suppresses MCF-7 tumour growth and bone metastasis in vivo by reducing tumour stromalizatio
194 ogic sympathetic activation on breast cancer bone metastasis in vivo can be blocked with the beta-blo
197 d whether MAF amplification (a biomarker for bone metastasis) in primary tumours could predict the tr
198 ltivariate logistic regressions on liver and bone metastasis, in which the number of involved nodes w
200 ysis revealed several potential mediators of bone metastasis, including the pyrophosphate-generating
201 h in vivo in a SCID-hu model of experimental bone metastasis induced by C4-2b prostate cancer cells.
208 omas such as breast cancer, where osteolytic bone metastasis is associated with increased morbidity a
209 omical site of breast cancer metastasis, and bone metastasis is associated with increased morbidity a
211 l's acquisition of properties for successful bone metastasis is influenced by signals from the stroma
215 Critical to our ability to prevent and treat bone metastasis is the identification of the key factors
216 mmon sites of distant metastases, and spinal bone metastasis is the most common source of neurologica
218 Knockdown of DLC1 in cancer cells promoted bone metastasis, leading to manifested osteolysis and ac
221 such differences, we established an ex vivo bone metastasis model, termed bone-in-culture array or B
224 ed osteolysis in an orthotopic breast cancer bone metastasis mouse model using FGFR non-amplified MDA
225 ovariectomy-induced osteoporosis, as well as bone metastasis of breast and skin cancers, are diminish
227 kappaB and found that it mediates osteolytic bone metastasis of breast cancer by stimulating osteocla
228 ppaB) plays a crucial role in the osteolytic bone metastasis of breast cancer by stimulating osteocla
232 In addition to its inhibitory effect on bone metastasis of Jagged1-expressing tumor cells, 15D11
233 ncluding (1) COX-2 transfection enhanced the bone metastasis of MDA-435S cells and (2) breast cancer
237 blood monocytes isolated from patients with bone metastasis of prostate cancer were more efferocytic
240 RANKL monoclonal antibody, for prevention of bone metastasis or death in non-metastatic castration-re
243 ence suggesting RANKL inhibition might delay bone metastasis or disease recurrence in patients with e
245 agnosis ( P = .02), higher rate of liver and bone metastasis ( P </= .02), shorter relapse-free survi
246 dge of the prognostic factors of PCa and the bone metastasis pattern of patients would be helpful for
248 characterized by solid histology, liver and bone metastasis, poor prognosis, and potential responsiv
249 k factors were assessed: sex, age over 70 y, bone metastasis, prior chemotherapy, prior external-beam
250 nodeficient mouse model of extravasation and bone metastasis produced detectable, progressive osteoly
252 on-resistant prostate cancer at high risk of bone metastasis (prostate-specific antigen [PSA] >/=8.0
254 ER mutations, especially their enrichment in bone metastasis, raised even more provocative questions
261 the mechanism of MMP13-dependent osteolytic bone metastasis revealed that MMP13-ASO treatment decrea
262 regarding risk factors for lung, liver, and bone metastasis, risk stratification is liable to be hap
263 Metastatic prostate cancer cell lines and bone metastasis samples displayed robust fetuin-A expres
265 routine MR imaging protocol for node and/or bone metastasis screening, which included coronal two-di
266 n for prevention of osteoclastic activity of bone metastasis, secondary to breast cancer, was identif
267 om control or tumor-bearing mice that lacked bone metastasis, signifying the essential cross-talk bet
268 The tumor-associated osteoblasts in PCa bone metastasis specimens and patient-derived xenografts
269 levels, Gleason scores, marital statuses and bone metastasis statuses was compared by Kaplan-Meier an
270 ts with different socioeconomic statuses and bone metastasis statuses was compared by Kaplan-Meier an
272 nt determined by time to first occurrence of bone metastasis (symptomatic or asymptomatic) or death f
273 the IL-11Ralpha-targeted proapoptotic agent bone metastasis-targeting peptidomimetic (BMTP-11) in pr
275 PDX) of castration-resistant prostate cancer bone metastasis that we exploited as a model of AVPC.
276 ediated anticancer drug delivery to sites of bone metastasis, thereby inhibiting cancer progression a
277 e show that olaparib increases breast cancer bone metastasis through PARP2, but not PARP1, specifical
278 in vivo in an immunodeficient mouse model of bone metastasis through upregulation of MMP2, but not MM
280 g tumor cells, 15D11 dramatically sensitizes bone metastasis to chemotherapy, which induces Jagged1 e
281 of breast cancer which exhibits spontaneous bone metastasis to evaluate the function and therapeutic
282 r cell line MDA PCa 2b, derived from a human bone metastasis, to generate an invasive subline (MDA-I)
284 and discuss new avenues of investigation for bone metastasis treatment based on current knowledge.
285 In an intratibial model of breast cancer bone metastasis, treatment with GANT58-NPs decreased bon
286 1alpha was detected in the hypoxic region of bone metastasis tumors in a mouse model of human melanom
287 (P < 0.0001) and also between patients with bone metastasis versus patients with soft-tissue metasta
288 nt differences in survival for patients with bone metastasis versus soft-tissue or no metastasis for
289 by cytotoxic chemotherapy can contribute to bone metastasis via a transient increase in bone marrow
290 ependent on tumor grade, and the presence of bone metastasis was associated with worse overall surviv
291 c and genotypic alterations before and after bone metastasis, we conducted genome-wide mRNA profiling
292 immunocompetent mouse model of breast cancer bone metastasis, we confirmed that MDSC isolated from th
293 mmunocompetent mouse models of breast cancer bone metastasis, we identified a key role for pDC in fac
296 Multiple BM and the presence of liver or bone metastasis were independent adverse prognostic fact
297 atus, higher PSA level, T1 and N0 stage, and bone metastasis were independent risk factors for increa
298 ents with renal cell carcinoma (RCC) develop bone metastasis, which is characterized by extensive ost
300 n of CD97 in PC3 cells resulted in decreased bone metastasis without affecting subcutaneous tumor gro