ライフサイエンスコーパス: lung metastases

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

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

3 st the development of colorectal cancers and lung metastases.

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

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

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

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

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

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

10 d form neither primary orthotopic tumors nor lung metastases.

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

12 ound necessary for subsequent development of lung metastases.

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

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

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

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

17 been implicated recently in the promotion of lung metastases.

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

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

20 ignaling pathway were overexpressed in early lung metastases.

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

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

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

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

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

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

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

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

29 , and adoptively transferred to mice bearing lung metastases.

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

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

32 ell as increased circulating tumor cells and lung metastases.

33 ediatric thyroid cancer patient with diffuse lung metastases.

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

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

36 linically obtained hormone receptor negative lung metastases.

37 l transitions to spindle cell carcinomas and lung metastases.

38 s CXCR3 which facilitates the development of lung metastases.

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

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

41 le, in pediatric patients exhibiting diffuse lung metastases.

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

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

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

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

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

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

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

49 d overall survival in mice with experimental lung metastases.

50 a formation and regulates the development of lung metastases.

51 42% of mice treated with WT cells developed lung metastases.

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

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

54 ntly reducing the incidence of extravascular lung metastases.

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

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

57 ive pressures on the development of liver or lung metastases.

58 cing tumor cell motility, intravasation, and lung metastases.

59 tly reduced the growth of primary tumors and lung metastases.

60 owth but severely decreased the formation of lung metastases.

61 the complete regression of 3-day established lung metastases.

62 an survival time of mice bearing established lung metastases.

63 and strongly suppresses the growth of Lewis lung metastases.

64 T cells to the B16 OVA melanoma, growing as lung metastases.

65 correlated with the extent of lymph node and lung metastases.

66 twofold to fivefold decrease in spontaneous lung metastases.

67 y correlated with reduction in the number of lung metastases.

68 od, individual tumor cells in the lungs, and lung metastases.

69 mammary cancer with about a 15% incidence of lung metastases.

70 a maximum of 100-fold decrease in clonogenic lung metastases.

71 moresistance and the high propensity to form lung metastases.

72 tigated the production of Chi3l1 in melanoma lung metastases.

73 cells were more susceptible to B16 melanoma lung metastases.

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

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

76 5aR-deficient mice were sufficient to reduce lung metastases.

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

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

79 vessel surfaces and increased the number of lung metastases.

80 rogates CTC cluster formation and suppresses lung metastases.

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

82 anscriptionally controlled miR-138 levels in lung metastases.

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

84 esistance to carcinogenesis and experimental lung metastases.

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

86 and mutant PIK3CA also cooperated to promote lung metastases.

87 s effective against distant solid tumors and lung metastases.

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

89 tumor growth, metastatic axillary tumors and lung metastases.

90 ors more efficiently formed mammospheres and lung metastases.

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

92 omy was performed for resection of bilateral lung metastases.

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

94 observed no variation in proliferation among lung metastases.

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

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

97 (5 vs. 7 vs. 15), and differences in size of lung metastases (1.2 vs. 1.4 vs. 1.0 mm diameter) compar

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

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

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

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

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

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

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

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

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

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

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

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

110 -established grossly detectable experimental lung metastases and advanced ascites tumors.

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

112 including a propensity for the formation of lung metastases and high vascularity.

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

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

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

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

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

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

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

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

121 results in the growth of previously dormant lung metastases and suggests that combining angiogenesis

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

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

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

125 antable mouse kidney tumors), propensity for lung metastases, and hypervascularity may make these tum

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

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

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

129 However, lung metastases appeared in 23% of the immunized mice wi

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

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

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

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

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

135 vivo studies, animals with well-established lung metastases (at least five nodules of 1 mm in diamet

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

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

138 with increased cell proliferation in B16-BL6 lung metastases but with decreased cell proliferation in

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

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

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

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

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

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

145 f a perineural invasion, a lymph node, and a lung metastases compared to that in normal or benign hyp

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

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

148 a dose-dependent reduction in the number of lung metastases compared with vehicle controls.

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

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

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

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

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

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

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

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

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

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

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

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

161 invade through Matrigel in vitro and to form lung metastases following intravenous injection in nude

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

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

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

165 eatment added to IR reduces proliferation of lung metastases from LLC primary tumors.

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

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

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

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

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

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

172 injection into immunodeficient mice, yielded lung metastases in 100% of animals.

173 astasize and in selected variants that cause lung metastases in 16 weeks (LM2) or 8 weeks (LM6) after

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

175 munity, as well as significant inhibition of lung metastases in a 3-day tumor model.

176 tumor challenge, and significantly inhibited lung metastases in a 3-day tumor model.

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

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

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

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

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

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

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

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

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

186 1 (BRMS1) inhibits formation of macroscopic lung metastases in breast, ovary, and melanoma xenograft

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

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

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

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

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

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

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

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

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

196 cells produced more and larger experimental lung metastases in NOS II+/+ mice than in NOS II-/- mice

197 ells produced fewer and smaller experimental lung metastases in NOS II+/+ mice than in NOS II-/- mice

198 r xenografts and inhibited A549 experimental lung metastases in nu/nu mice.

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 invasion in vitro and increased experimental lung metastases in vivo.

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

212 ramatically suppressed their ability to form lung metastases in vivo.

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

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

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

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

217 dium (CM) obtained from histocultures of rat lung metastases induced a 3-fold resistance.

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

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

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

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

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

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

224 ate the treatment of established CT26 or B16 lung metastases, mice were treated with cultured dendrit

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

226 Using an OVA-transfected B16 lung metastases model, we assessed the therapeutic effec

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

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

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

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

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

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

233 ely suppressed dissemination of experimental lung metastases of CT26-KSA colon carcinoma in syngeneic

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

235 entiated tumor cells but strongly suppresses lung metastases of more aggressive carcinoma cells after

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

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

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

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

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

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

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

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

244 sseminated metastatic cells was relieved and lung metastases progressed.

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

246 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

247 A cell line that is established from lung metastases releases more IL-8, has a higher cloning

248 These lung metastases remained refractory to treatment despite

249 Significant inhibition of established lung metastases required immunization with peptide-pulse

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

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

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

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

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

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

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

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

258 e exhibited more circulating tumor cells and lung metastases than Neu mice, while NT tumors contained

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

278 Lung metastases were also significantly decreased in the

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

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

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

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

283 More frequent lung metastases were observed in naive recipients given

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

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

286 Number and size of lung metastases were significantly increased.

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

288 Lung metastases were simulated as spheres, with radii ra

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

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

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

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

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

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

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

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

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

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

299 h phase in situ and give rise to spontaneous lung metastases within 10 weeks.

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