ライフサイエンスコーパス: lung metastases

1 asive activity and ability to form liver and lung metastases.

2 o naive mice to inhibit aggressive growth of lung metastases.

3 vessel surfaces and increased the number of lung metastases.

4 rogates CTC cluster formation and suppresses lung metastases.

5 ectopic miR-15a/16-1 suppressed formation of lung metastases.

6 anscriptionally controlled miR-138 levels in lung metastases.

7 esistance to carcinogenesis and experimental lung metastases.

8 the tumor, draining lymph nodes, spleen, and lung metastases.

9 and mutant PIK3CA also cooperated to promote lung metastases.

10 lutarate production in breast-cancer-derived lung metastases.

11 ed early stage non-small-cell lung cancer or lung metastases.

12 tumor growth, metastatic axillary tumors and lung metastases.

13 ors more efficiently formed mammospheres and lung metastases.

14 d lesion as well as the distant B16 melanoma lung metastases.

15 es were used to treat mice with pre-existing lung metastases.

16 observed no variation in proliferation among lung metastases.

17 etastases, whereas CT was more sensitive for lung metastases.

18 ction in both tumor growth and the number of lung metastases.

19 pic 4T1 mammary carcinomas, and reducing 4T1 lung metastases.

20 st the development of colorectal cancers and lung metastases.

21 d to a dramatic increase in the formation of lung metastases.

22 R2 on primary tumour growth and experimental lung metastases.

23 rs and inhibited the development of TRAMP-C1 lung metastases.

24 mors develop large numbers of lymph node and lung metastases.

25 cell numbers in, and suppression of, B16F10 lung metastases.

26 sing the BMPR2-DN had a fivefold increase in lung metastases.

27 d form neither primary orthotopic tumors nor lung metastases.

28 responsible for anti-gp75 mAb therapy of B16 lung metastases.

29 ound necessary for subsequent development of lung metastases.

30 to reduce tumor volume, local invasion, and lung metastases.

31 tivation activity, primary tumor growth, and lung metastases.

32 ancer cells, markedly reducing the number of lung metastases.

33 on reduces both tumor size and the number of lung metastases.

34 tumor resistance to fulvestrant and induced lung metastases.

35 t they inhibited formation of both liver and lung metastases.

36 e degradation or the formation and growth of lung metastases.

37 ignaling pathway were overexpressed in early lung metastases.

38 the treatment of patients with one to three lung metastases.

39 blood vessels; however, neither cells formed lung metastases.

40 flammation resulted in a >3-fold increase in lung metastases.

41 . inoculated, only non-EMT cells established lung metastases.

42 anks of normal mice and mice bearing MCA 205 lung metastases.

43 These changes were associated with lung metastases.

44 an increased frequency, number, and size of lung metastases.

45 nce of asthma was higher among patients with lung metastases.

46 , and adoptively transferred to mice bearing lung metastases.

47 gation as a therapy for cancer patients with lung metastases.

48 erived from vMCF-7(DNp53) cells gave rise to lung metastases.

49 ell as increased circulating tumor cells and lung metastases.

50 ediatric thyroid cancer patient with diffuse lung metastases.

51 n-TAK1 reduces tumor growth and formation of lung metastases.

52 as advantages over (90)Y in treating smaller lung metastases.

53 linically obtained hormone receptor negative lung metastases.

54 l transitions to spindle cell carcinomas and lung metastases.

55 s CXCR3 which facilitates the development of lung metastases.

56 hat developed, nor in the propensity to form lung metastases.

57 le, in pediatric patients exhibiting diffuse lung metastases.

58 nd CpG reduced the number of B16F10 melanoma lung metastases.

59 APCs) to enhance anticancer immunity against lung metastases.

60 lung toxicity in the presence of iodine-avid lung metastases.

61 mice developed peritoneal carcinomatosis and lung metastases.

62 or the formation of parental 4T1 spontaneous lung metastases.

63 T+/- TK-/- mice developed mammary tumors and lung metastases.

64 ed the formation of spontaneous parental 4T1 lung metastases.

65 a patient), later resulted in both bone and lung metastases.

66 entage of MMP-3 null mice evidencing surface lung metastases.

67 d overall survival in mice with experimental lung metastases.

68 reduce the metastatic lesions in established lung metastases.

69 42% of mice treated with WT cells developed lung metastases.

70 ral pregnancies, some of which progressed to lung metastases.

71 ntly reducing the incidence of extravascular lung metastases.

72 cells that are essential for the control of lung metastases.

73 mice harboring LCC6-DN xenografts showed no lung metastases.

74 eg cells were detected in close proximity to lung metastases.

75 d an invasive phenotype and formed liver and lung metastases.

76 ion, although slight progression of bone and lung metastases.

77 ion of the pre-metastatic niche and melanoma lung metastases.

78 deletion had a greater incidence and larger lung metastases.

79 mmatory tumor microenvironment in multifocal lung metastases.

80 g wild-type-like properties in prevention of lung metastases.

81 s effective against distant solid tumors and lung metastases.

82 omy was performed for resection of bilateral lung metastases.

83 g marked inhibition of both tumor growth and lung metastases.

84 posure, and dramatically reduces CTC-derived lung metastases.

85 been implicated recently in the promotion of lung metastases.

86 t engrafted or spontaneous tumors as well as lung metastases.

87 Compared with IgG, anti-FRalpha IgE reduced lung metastases.

88 , neutrophils, and inflammatory monocytes to lung metastases.

89 g with PET/MRI bears a risk of missing small lung metastases.

90 a formation and regulates the development of lung metastases.

91 ior to CVX-241 as treatment for postsurgical lung metastases.

92 twofold to fivefold decrease in spontaneous lung metastases.

93 moresistance and the high propensity to form lung metastases.

94 tigated the production of Chi3l1 in melanoma lung metastases.

95 cells were more susceptible to B16 melanoma lung metastases.

96 ons, reduced tumor vascularization, and less lung metastases.

97 tastasis, leading to protection of mice from lung metastases.

98 5aR-deficient mice were sufficient to reduce lung metastases.

99 HCC and, in some cases, hepatoblastomas and lung metastases.

100 (5 vs. 7 vs. 15), and differences in size of lung metastases (1.2 vs. 1.4 vs. 1.0 mm diameter) compar

101 ssion also increased by 3-fold the number of lung metastases 14 days after tail vein injection of tum

102 /CT trended toward increased sensitivity for lung metastases (20 of 23 [87%] for reader 1 and 17 of 2

103 frequency of liver (63% v 82%, P < .001) and lung metastases (27% v 34%, P = .01).

104 Of the 1,687 patients analyzed, 5.7% had lung metastases, 4.8% had bone involvement, and 6% had b

105 BM involvement increased in the presence of lung metastases (41% with, 6% without).

106 ectively), whereas sensitivity was lower for lung metastases (48.3% vs. 100% and 75.9%, respectively)

107 The number of lung metastases (5+/-1/mouse) was much lower than in AQP

108 ion for hematogenous metastasis, we examined lung metastases after intravenous injection of melanoma

109 after mammary orthotopic reinjection and of lung metastases after tail vein injection.

110 brogated the capacity of these cells to form lung metastases after tail-vein injection, whereas mTerc

111 e observed objective regression of all seven lung metastases after the infusion of approximately 1.11

112 established PANC-1 tumors and inhibited A549 lung metastases, all without apparent toxicity.

113 yrp1 DNA vaccination in the treatment of B16 lung metastases, an effect mediated by immunologic mecha

114 expressed on 14 of 16 osteosarcoma patients' lung metastases and four different human osteosarcoma ce

115 h alpha-TEA-generated autophagosomes reduced lung metastases and increased the survival of tumor-bear

116 tor T cells was measured by the reduction in lung metastases and is shown to be dose dependent.

117 Enriched sgRNAs in lung metastases and late-stage primary tumors were found

118 r (PC) patients, the differentiation between lung metastases and lesions of different origin, for exa

119 ate antitumor immunity, leading to increased lung metastases and mortality.

120 recurrence in patients treated with RFA for lung metastases and primary lung cancers.

121 n modification of Bcl-x pre-mRNA splicing in lung metastases and reduced tumor load, while nanopartic

122 at a faster rate, than KC mice, and had more lung metastases and significantly shorter average surviv

123 present a risk factor for the development of lung metastases and suggest that amelioration of the pul

124 role for MMP-12 in suppressing the growth of lung metastases and suggest that inhibitors designed to

125 el, systemically delivered MSCs localized to lung metastases and the controlled local delivery of TRA

126 d conferring long-term survival in mice with lung metastases and with repeated tumor challenge.

127 became resistant to this drug (emergence of lung metastases) and died shortly thereafter.

128 transduced melanoma cells, and tumor growth, lung metastases, and histology were characterized.

129 model is applicable to subcutaneous tumors, lung metastases, and intracranial tumors and offers a so

130 emotaxis/invasion in vitro, WM266.4 melanoma lung metastases, and lymphatic metastases from orthotopi

131 rmed the loss of Bsp protein in 1D11-treated lung metastases, and TGF-beta was shown to regulate and

132 However, lung metastases are a frequent finding in oncologic pati

133 t CD44(+) cells from both primary tumors and lung metastases are highly enriched for tumor-initiating

134 Bone and lung metastases are responsible for the majority of deat

135 STAT3 signaling pathways was observed in the lung metastases as compared to the primary tumors.

136 ted dramatic enhancement in the formation of lung metastases as compared with parental cells.

137 eased latency and reduced growth, with fewer lung metastases, as compared with Hic-5(+/-);PyMT mice.

138 fts (L1210 and L1210-10K leukemia cells) and lung metastases (B-16 melanoma cells) was measured on sm

139 ility of IL-2/alpha-CD40 treatment to reduce lung metastases but had no effect on primary tumor burde

140 We discovered that breast-cancer-derived lung metastases, but not the corresponding primary breas

141 in wildtype cells of both primary tumors and lung metastases, but, surprisingly, MT1-MMP deficiency d

142 weeks in PyVmT mice decreased the number of lung metastases by >10-fold (P<0.06) without a detectabl

143 hibited growth of RenCa renal cell carcinoma lung metastases by 26%, whereas VEGFR-1 antibody (MF-1)

144 rostate cancer cells increased the number of lung metastases by 33-fold in an experimental metastasis

145 genistin treatment, significantly inhibited lung metastases by 95% (P < 0.01) associated with signif

146 anoma cells in vitro and the colonization of lung metastases by B16-F10 murine melanoma cells in C57B

147 sed E-cadherin expression, and yielded fewer lung metastases compared to control.

148 lar density and an increase in the number of lung metastases compared with C1qa(-/-) mice.

149 sion of primary tumor growth and spontaneous lung metastases compared with controls.

150 also demonstrated a significant reduction in lung metastases compared with wild-type mice.

151 In Spp1(-/-) mice, the inhibition of lung metastases correlated with the expansion of granulo

152 deficiency delayed tumor growth and reduced lung metastases, correlating with a reduction in phospho

153 The vast majority of examined liver and lung metastases derived from a colorectal cancer cell li

154 This imaging method was evaluated in lung metastases derived from human MDA-MB-231 breast can

155 ice sacrificed 5 weeks later showed multiple lung metastases derived from LCC-WT xenografts, whereas

156 In these doubly transgenic mice, lung metastases developed with characteristics of the pr

157 In vivo, lung metastases developing from orthotopic MDA-MB-231 tu

158 all of his cutaneous tumors shrank, but his lung metastases did not.

159 cells, mice lacking PITPalpha develop fewer lung metastases due to a reduction of fibrin formation s

160 ancreatic islet cancers, mammary tumors, and lung metastases during malignant progression.

161 monophosphate (NP-cGAMP) in mouse models of lung metastases enables rapid distribution of NP-cGAMP t

162 quency of development of prostate cancer and lung metastases, even when the mice were treated after t

163 CDK5 had less than one-fourth the number of lung metastases exhibited by AT6.3 cells expressing the

164 A patient with three lung metastases experienced complete regression of one t

165 munocompetent rat model system of rat tumour lung metastases expressing human FRalpha, and engineered

166 a cell line strongly suppressed formation of lung metastases following tail vein injection.

167 PU17) in most primary iUC and many nodal and lung metastases from dogs, and scintigraphy confirmed fo

168 ctal cancers as well as coexisting liver and lung metastases from individual patients suggests that i

169 and function of TILs derived from liver and lung metastases from patients with gastrointestinal (GI)

170 In vivo tumor control of B16F10 lung metastases further confirmed the variant DTT-IYG to

171 TGF-beta1 for as little as 2 weeks increased lung metastases >10-fold without a detectable effect on

172 Patients who had only lung metastases had EFS and S of 32% (SE, 8%) and 41% (S

173 The ability of osteosarcoma cells to form lung metastases has been inversely correlated to cell su

174 Finally, TNBC lung metastases have lower LD abundance than their corre

175 V-induced pre-metastatic niche, and melanoma lung metastases; however, ablation of Ch25h reversed the

176 tabine) after the diagnosis of new liver and lung metastases in 2010, irinotecan in 2011, and then ce

177 clones into immunocompetent mice resulted in lung metastases in 50% and 80% of mice respectively, whe

178 th and vascularization of primary tumors and lung metastases in a breast cancer xenograft model as we

179 E) cannot be phosphorylated are resistant to lung metastases in a mammary tumor model, and that cells

180 eously arising primary mammary carcinoma and lung metastases in a mouse tumor model in vivo.

181 growth but markedly suppresses formation of lung metastases in a sequence-specific manner.

182 hed the ability of human tumor cells to form lung metastases in a xenograft model.

183 ontin (Opn) expression in WAP-HGF tumors and lung metastases in agreement with a previously reported

184 murine models and reduced the development of lung metastases in an invasive model.

185 Increased lung metastases in animals fed a Western-type diet were

186 er cells suppressed formation of macroscopic lung metastases in both spontaneous and experimental mod

187 1 (BRMS1) inhibits formation of macroscopic lung metastases in breast, ovary, and melanoma xenograft

188 ppresses the ability of B16F10 cells to form lung metastases in C57Bl/6 syngeneic mice.

189 onset and progression of mammary tumors and lung metastases in female mice over a 14-week period.

190 lung cancer cells and enhances experimental lung metastases in immunodeficient as well as immunocomp

191 tivating kinase (ULK1) mutant K46N increased lung metastases in MDA-MB-231 xenograft mouse models.

192 Radiation failed to enhance lung metastases in mice bearing tumors that lack the typ

193 apacity to invade Matrigel, and ability form lung metastases in mice following tail-vein injection.

194 incubated with PGE(2) formed more liver and lung metastases in mice than control LS174T cells.

195 We next treated clinically detectable lung metastases in mice with anti-CD24 antibody and obse

196 e ability of pancreatic cancer cells to form lung metastases in mice.

197 c potential of (90)Y and (131)I targeting of lung metastases in NHL patients.

198 h faster and produced many more experimental lung metastases in NOS II(-/-) mice than in NOS II(+/+)

199 sfer of P1A-specific CTL effectively treated lung metastases in syngeneic mice challenged with P1A-ne

200 Bioluminescent in vivo imaging revealed that lung metastases in T24T grew faster than the same tumors

201 roughly 2-fold decrease in the incidence of lung metastases in Tg mice (33.3%) compared to WT mice (

202 aling lipid phosphatidic acid (PA), inhibits lung metastases in the mammary tumor virus (MMTV)-Neu tr

203 in TAMs decreased the frequency and size of lung metastases in three different mouse models of breas

204 ng to abrogated growth of primary tumors and lung metastases in tumor xenograft assays.

205 osh significantly increased the incidence of lung metastases in tumor-bearing animals compared with m

206 into NK-deficient mice and observed enhanced lung metastases in tumor-bearing mice as compared with m

207 suppress the growth of tumor xenografts and lung metastases in vivo and rendered it susceptible to r

208 lso decreased the formation of breast cancer lung metastases in vivo, and breast cancer cells derived

209 wn in the bone marrow significantly impaired lung metastases in vivo, without impacting their recruit

210 growth and development of breast tumors and lung metastases in vivo.

211 invasion in vitro and increased experimental lung metastases in vivo.

212 l invasiveness in vitro and tumor growth and lung metastases in vivo.

213 rol of subcutaneously growing tumors but not lung metastases; in contrast, using immunized asplenic m

214 subcutaneous tumors were unable to generate lung metastases, indicating in vivo functional differenc

215 eloid cell-selective KO of Atf3 showed fewer lung metastases, indicating that host ATF3 facilitates m

216 tely eliminated 4T1 breast cancer growth and lung metastases induced by 4T1 cells in mice when treatm

217 es little additional benefit if the risk for lung metastases is low.

218 However, the presence of lung metastases is markedly suppressed in Muc4(ko)/NDL m

219 indicate that the primary role of tBregs in lung metastases is to induce TGF-beta-dependent conversi

220 py model using bioluminescent measurement of lung metastases loads, novel mouse strains, and anti-Fcg

221 Notably, lung metastases mainly consist of non-EMT tumour cells t

222 y vector-transduced B16 cells produced large lung metastases, miR-21 knockdown cells only formed smal

223 Focusing on the amenable B16F10 experimental lung metastases model, we determined that expression of

224 Using an OVA-transfected B16 lung metastases model, we show that adoptively transferr

225 rved in several experimental and spontaneous lung metastases models as well as in models of de novo c

226 Patients with KRAS mutation had lung metastases more frequently than wtKRAS individuals

227 ation were larger, grew faster and developed lung metastases more readily.

228 rentiated, luminal-type breast adenomas with lung metastases [mouse mammary tumor virus-driven polyom

229 Here we show that liver and lung metastases of human breast cancers tend to be highl

230 Our data find correlation with lung metastases of human mammary carcinomas that are ass

231 via administration directly to the sites of lung metastases of osteosarcoma.

232 and had an even greater antitumor effect on lung metastases of the same mice, which was dependent on

233 sion properties, in targeted therapy for NHL lung metastases of various nodule sizes and tumor burden

234 cancer (PDX models) that exhibit spontaneous lung metastases offer a potentially powerful model of ca

235 BALB/c mice bearing murine CT26 colon tumor lung metastases or palpable s.c. tumors (>100 mm(3)) wit

236 or weight loss, breathing problems linked to lung metastases or pathologic fractures.

237 ssion of irradiated tumors and nonirradiated lung metastases or synchronous tumors (abscopal effect).

238 and presence or absence of liver metastases, lung metastases, or both.

239 Lung metastases (P < 0.0001) and single-site metastases

240 gonadotropin > or = 1,000 U/L (P = .01), and lung metastases (P = .02) significantly predicted advers

241 sseminated metastatic cells was relieved and lung metastases progressed.

242 or subcutaneous xenografts (r(2) = 0.93) and lung metastases (r(2) = 0.83).

243 e, 4-12 mm; mean +/- SD, 6.1 +/- 1.7 mm) and lung metastases (range, 1-5 mm; mean, 2.1 +/- 1.2 mm) we

244 These lung metastases remained refractory to treatment despite

245 npulsed DCs induced protection against tumor lung metastases resulting from i.v. injection of a synge

246 ysis of the unique molecular features of the lung metastases revealed a significant association with

247 , and breast cancer cells derived from mouse lung metastases showed enhanced Ser 178 paxillin phospho

248 tagonism resulted in a dramatic reduction of lung metastases, similar to the effect of reexpressing R

249 ich facilitated development of liver but not lung metastases, suggesting that ANGPT2 and CXCR4 are im

250 MP7 also had no effect on the development of lung metastases, suggesting that MMP7 is irrelevant in t

251 mors, prostate tumors, colon xenografts, and lung metastases, TAMs expressed argI(high)iNOS(low) earl

252 expressing collagen XXIII shRNA formed fewer lung metastases than control cells.

253 cases, DNMP mice were less likely to develop lung metastases than controls.

254 odies more potently decreased lymph node and lung metastases than each antibody alone.

255 KK4(-/-) clones injected i.v. produced fewer lung metastases than syngeneic MKK4-competent cells (P =

256 ic mice resulted in larger and more frequent lung metastases than transplantation of control cells.

257 simetry of thyroid cancer patients with avid lung metastases that exhibit prolonged retention in the

258 Overall, under conditions of extensive lung metastases, these data revealed for the first time

259 nd inhibits both the formation and growth of lung metastases through its selective effect on myeloid-

260 metastases are more reliant on VEGFR-1 than lung metastases to mediate angiogenesis due to different

261 Interestingly, in the experimental lung metastases tumor models, we observed that intracell

262 ay a cancer "stem-like" phenotype by forming lung metastases under limiting cell dilution.

263 nt with ICOS-Fc inhibited the development of lung metastases upon injection of NOD-SCID-IL2Rgammanull

264 ifferences between primary tumors and paired lung metastases using a syngeneic p53-null mammary tumor

265 s are exposed to these factors ubiquitously, lung metastases usually develop as a series of discrete

266 tumors (as stimulator in bladder, kidney and lung metastases vs as suppressor in prostate and liver m

267 The accuracy in diagnosing lung metastases was 98.3% for dedicated CT versus 97.4%

268 ediatric thyroid cancer patient with diffuse lung metastases was administered 37 MBq of (131)I after

269 However, the incidence of lung metastases was dramatically reduced.

270 y a striking 87% (P < 0.05) and incidence of lung metastases was inhibited by 83% (P < 0.02).

271 the ability of B16F10 melanoma cells to form lung metastases was significantly reduced in Cav1KO mice

272 than QRsP-11 cells, whereas the incidence of lung metastases was similar to that of QRsP-11 cells.

273 he formation of spontaneous and experimental lung metastases was strongly decreased in DEP-1-deficien

274 In studying the development of lung metastases, we found that NK cells lose their cytot

275 Lung metastases were also observed in a VEGF-dependent m

276 Lung metastases were also significantly decreased in the

277 Lung metastases were counted in wild-type (WT) and CCR5(

278 ng conventional imaging (P = .03), but fewer lung metastases were detected (P < .001).

279 Lung metastases were found in 75% of Sulf1-Tg mice but n

280 More strikingly, lung metastases were observed at this time in 55% of the

281 More frequent lung metastases were observed in naive recipients given

282 umber, vessel number or vessel structure and lung metastases were observed with similar frequency and

283 Surprisingly, we found that lung metastases were predominantly derived from the epit

284 Bone, lymph node, liver, and lung metastases were present in 99%, 65%, 17%, and 11% o

285 h of primary tumors and numbers of liver and lung metastases were quantified and analyzed by histolog

286 re injected into the tail veins of mice, and lung metastases were quantified.

287 into immune-competent and NOD/SCID mice, and lung metastases were quantified.

288 In addition, the numbers of lung metastases were significantly reduced in both exper

289 Lung metastases were simulated as spheres, with radii ra

290 Both s.c. implanted tumors and lung metastases were susceptible to anti-FAP immunothera

291 important in the treatment of patients with lung metastases when a recombinant human thyroid-stimula

292 ntrast, no difference was seen in numbers of lung metastases when comparing TRAIL(-/-) and WT mice, s

293 l line reduced tumor growth and experimental lung metastases when the cells were transplanted into mi

294 was often detected as small, slowly growing lung metastases, whereas progression of nonresectable li

295 tion was sufficient to decrease experimental lung metastases, which suggests that its role in endothe

296 e that TGF-beta can promote the formation of lung metastases while impairing Neu-induced tumor growth

297 ion in a mouse breast cancer model increases lung metastases, while reducing Zeppo1 expression reduce

298 te liver metastases or tail vein to generate lung metastases with sequential progeny derived by re-in

299 There were significantly fewer lung metastases with SMEL/IL-1ra versus SMEL (P < 0.002)

300 e prodrug eliminated primary tumor cells and lung metastases without apparent toxicity.