ライフサイエンスコーパス: lung metastasis

1 r growth, reduced vascularity, and decreased lung metastasis.

2 expression in control tumor cells suppressed lung metastasis.

3 educed growth of primary tumors but enhanced lung metastasis.

4 s able to induce a marginal reduction of B16 lung metastasis.

5 or V2 with GIT1 further enhanced growth and lung metastasis.

6 al transition as well as fibrin invasion and lung metastasis.

7 ased the occurrence of vascular invasion and lung metastasis.

8 epithelial-mesenchymal transition (EMT) and lung metastasis.

9 l recurrence, peritoneal carcinomatosis, and lung metastasis.

10 which encode proteins that are required for lung metastasis.

11 the formation of highly malignant HCCs with lung metastasis.

12 e, and when injected into tail veins, led to lung metastasis.

13 ic vessel invasion (LVI), and lymph node and lung metastasis.

14 t cancer and found that it strongly promotes lung metastasis.

15 itiation, growth, latency, multiplicity, and lung metastasis.

16 t completely abrogate cancer progression and lung metastasis.

17 f mice with soluble JAM-C prevented melanoma lung metastasis.

18 as in metastatic melanoma including melanoma lung metastasis.

19 tarded MDA-MB-435 tumor growth and inhibited lung metastasis.

20 or anti-Bv8 antibodies significantly reduced lung metastasis.

21 erived cells (BMDCs) play a critical role in lung metastasis.

22 ure in the premetastatic lung and diminishes lung metastasis.

23 inhibition of tumor growth and experimental lung metastasis.

24 melanomas have a similar ability to suppress lung metastasis.

25 ortant contribution of plasma fibronectin in lung metastasis.

26 sed toxins or depleting Tregs and preventing lung metastasis.

27 of tumor burden in an experimental model of lung metastasis.

28 y inhibits tumor growth and the incidence of lung metastasis.

29 t tumors resulted in significant blockage of lung metastasis.

30 asiveness in vivo and in vitro, and increase lung metastasis.

31 al of the primary tumor and (3) incidence of lung metastasis.

32 arable mammary tumors had significantly less lung metastasis.

33 reast cancer with a high risk for developing lung metastasis.

34 otably, ablation of Gab2 severely suppressed lung metastasis.

35 inhibiting tumor angiogenesis and prevented lung metastasis.

36 s prostate tumor growth and the incidence of lung metastasis.

37 ration of AMG487 also inhibited experimental lung metastasis.

38 ed significant differences in lymph node and lung metastasis.

39 icantly delayed tumor cell dissemination and lung metastasis.

40 etected in primary tumor, nodal disease, and lung metastasis.

41 ation and in vivo xenograft tumor growth and lung metastasis.

42 metastasis and moderately effective against lung metastasis.

43 e of lymph node metastasis while eliminating lung metastasis.

44 metastasis in an experimental mouse model of lung metastasis.

45 el, results in increased tumor formation and lung metastasis.

46 pair of primary renal cell carcinoma and its lung metastasis.

47 d Akt2(-/-) mice display a high incidence of lung metastasis.

48 , ultimately attenuating melanoma growth and lung metastasis.

49 ial, tumor-endothelial cell interaction, and lung metastasis.

50 kdown in transplanted NSCLC cells attenuated lung metastasis.

51 when tested in a mouse model of experimental lung metastasis.

52 rongly promoted both tumor cell invasion and lung metastasis.

53 eading to melanoma growth, angiogenesis, and lung metastasis.

54 ndothelial retraction required for efficient lung metastasis.

55 and MMP3 promoted melanoma tumor growth and lung metastasis.

56 of HCC cells along with tumor formation and lung metastasis.

57 bited significantly reduced tumor growth and lung metastasis.

58 ed suppression of ERK signaling and promotes lung metastasis.

59 tors that sustain CIC phenotypes and promote lung metastasis.

60 ransition and promotes tumor progression and lung metastasis.

61 a decreased capacity for tumor formation and lung metastasis.

62 47 in tumor growth and their requirement for lung metastasis.

63 ft model and clinical data validated IL-8 in lung metastasis.

64 tected Tsp-1 from degradation and suppressed lung metastasis.

65 Myc, the effect was markedly pronounced with lung metastasis.

66 endostatin did not significantly inhibit OS lung metastasis.

67 MMTV-PyMT mammary tumor cell lines enhances lung metastasis.

68 /E47-mediated modulation of tumor growth and lung metastasis.

69 and greatly increased the size and number of lung metastasis.

70 fer therapeutic benefits to prevent or treat lung metastasis.

71 displayed resistance to DEN-induced HCC and lung metastasis.

72 ft lower leg and foot, as well as a solitary lung metastasis (12 mm).

73 10 involved nodes indicated a small risk of lung metastasis [3%-4%; odds ratio (OR) 3-4], tumors gre

74 nty-two patients (10.1%) were diagnosed with lung metastasis, 58 patients (8.1%) with liver metastasi

75 ypoxia in promoting primary tumor growth and lung metastasis, a 45-gene hypoxia response signature ef

76 t that blockade of the ET-1 axis may prevent lung metastasis, a new therapeutic concept that warrants

77 from the radial growth phase (WM35) and from lung metastasis (A375-P).

78 ammary-injected, these cells did not exhibit lung metastasis after 21 days and caused only 40% lethal

79 miR-182 considerably increased, the rate of lung metastasis after amputation of the tumor-bearing li

80 One patient was found to have lung metastasis after HIFU and had an operation to remov

81 hy-1 showed markedly diminished experimental lung metastasis after injection of B16/F10 melanoma cell

82 mice showed markedly diminished experimental lung metastasis after injection of Lewis lung carcinoma

83 t reduction in tumor growth and experimental lung metastasis after PAR-1 silencing via systemic deliv

84 the sucrose was responsible for facilitating lung metastasis and 12-HETE production in breast tumors.

85 orroborated the role of host-derived MMP9 in lung metastasis and also facilitated determination of a

86 as platelet-derived P-selectin in promoting lung metastasis and also plays an important role in live

87 e that appears important for tumorigenicity, lung metastasis and cancer cachexia, and thus a promisin

88 FASN silencing enhanced lung metastasis and death in vivo.

89 his system as a useful tool for the study of lung metastasis and defines targets of therapy that may

90 tastases in an orthotopic xenograft model of lung metastasis and in an intracardiac injection model o

91 in patient tumors (n=92), is associated with lung metastasis and poor overall survival of osteosarcom

92 High ezrin expression is associated with lung metastasis and poor survival in cancer.

93 Treatment with DMH1 reduced lung metastasis and the tumors were less proliferative a

94 ed the number of cancer cells in xenografts, lung metastasis and then primary tumor growth was impair

95 ET-1 expression can serve as a biomarker for lung metastasis and whether it is required for metastati

96 atic carcinogenesis, haematogenous liver and lung metastasis, and cytomegalovirus infection.

97 tumor burden, prolonged survival, decreased lung metastasis, and decreased blood vessel density, whe

98 hangiogenesis and lymph node and spontaneous lung metastasis, and enhances survival.

99 b treatment, inhibited tumor growth, reduced lung metastasis, and improved survival.

100 d that MCPIP1 regulated ccRCC cell motility, lung metastasis, and mesenchymal phenotype by regulating

101 hylation as a potential molecular marker for lung metastasis, and suggest that epigenetic reversion o

102 3 on 66.1 tumor cells inhibited experimental lung metastasis, and this antimetastatic activity was co

103 cancer cells, biologic mechanisms regulating lung metastasis are not fully understood.

104 down of Ron expression significantly reduced lung metastasis as compared with the control cells in th

105 and number of metastases in an experimental lung metastasis assay.

106 We also noted a dramatic reduction in lung metastasis associated with decreased macrophage-med

107 ces in primary tumor growth and experimental lung metastasis between mice injected with Cl66-siVEGFC

108 nesis promotes both primary tumor growth and lung metastasis but is nonessential for bone metastasis.

109 ound to be organ specific, clearly enhancing lung metastasis but not affecting B16F1 liver metastasis

110 All WT/PyMT mice developed massive lung metastasis, but AIB1(-/-)/PyMT mice with comparable

111 st cancer patients with low or high risks of lung metastasis, but not for bone metastasis.

112 clotting cascade is selectively involved in lung metastasis, but the reason for this selectivity is

113 cell line increased primary tumor growth and lung metastasis by 2.5- and 3-fold, respectively, when i

114 ration in vitro, and suppressed experimental lung metastasis by 69% and 84%, respectively (mean +/- S

115 ed cell line, namely Met-1 cells, suppressed lung metastasis by approximately 4.5-fold.

116 contributes to breast cancer progression and lung metastasis by inducing several growth factors that

117 egs) play an essential role in breast cancer lung metastasis by inducing TGF-beta-dependent conversio

118 oles in the regulation of breast cancer cell lung metastasis by modulating cell morphology and cell i

119 berberine treatment reduced tumor growth and lung metastasis by oral gavage, respectively.

120 We show here that experimental lung metastasis by two cell lines, B16F1 melanoma and 3L

121 integrin alphavbeta3 and fibronectin promote lung metastasis by upregulating Slug, defining a mechani

122 fter arrest in the lung, during experimental lung metastasis, by recruiting macrophages characterized

123 Limitations in detecting lung metastasis can be overcome by using a hybrid PET/CT

124 a lower incidence and degree of invasion and lung metastasis compared with control animals.

125 esponse against B16 melanoma and its distant lung metastasis compared with unmodified Grp170 and flag

126 metalloproteases eliminated degradation and lung metastasis, consistent with a direct link among inv

127 The inhibition of lung metastasis correlated with reduced cancer cell migr

128 Hematogenous metastasis (blood tumor burden, lung metastasis) correlated with degree of lymph node in

129 Thus, transendothelial migration and lung metastasis development decreased by approximately 5

130 a cell extravasation in vitro and subsequent lung metastasis development in vivo.

131 a cell extravasation in vitro and subsequent lung metastasis development in vivo.

132 this study showing that neutrophils regulate lung metastasis development through physical interaction

133 ressing the microRNA miR-200 does not affect lung metastasis development.

134 K shRNA cells promoted Matrigel invasion and lung metastasis equal to 4T1 controls.

135 er of WT IMs increases the reduced number of lung metastasis foci in Ccl3 deficient mice.

136 or CCR1 in macrophages reduces the number of lung metastasis foci, as well as the number of MAMs accu

137 y reduced tumor incidence, tumor volume, and lung metastasis following intratibial injection.

138 ress fibers, migration using Transwells, and lung metastasis following tail vein inoculation.

139 cells significantly contribute to recurrent lung metastasis formation after chemotherapy.

140 at deletion of RXR in myeloid cells enhances lung metastasis formation while not affecting primary tu

141 ice and, thereby, restoring immunity against lung metastasis formation.

142 ss by either route also dramatically reduced lung metastasis formation.

143 d re-expression of VEGF only rescues partial lung metastasis formation.

144 with ERalpha-negative breast cancers and in lung metastasis-free breast cancers.

145 methylation in circulating tumor DNA reduced lung metastasis-free survival.

146 vasation of both cell types and formation of lung metastasis from non-EMT cells.

147 tically reduced the incidence of spontaneous lung metastasis from primary tumors and decreased tumor

148 soluble isoforms conferred an advantage for lung metastasis from subcutaneous tumors (fs120/164 vs.

149 cells results in increased intravasation and lung metastasis from tumors formed by injection of cells

150 this set of genes with a human breast cancer lung metastasis gene signature identified five common ta

151 hrough the analysis of a previously defined "lung metastasis gene-expression signature" (LMS) that me

152 TV-PyMT (PyMT), developed breast tumors with lung metastasis; however, mice deleted in p38delta (PyMT

153 ministration robustly inhibits breast cancer lung metastasis in a dose-dependent manner, associated w

154 mor cells in vitro but was found to increase lung metastasis in a mouse model of breast cancer metast

155 ung cancer cells and attenuates experimental lung metastasis in a xenograft mouse model.

156 miR-145 is also able to suppress lung metastasis in an experimental metastasis animal mod

157 we find that Lamellipodin depletion reduced lung metastasis in an orthotopic mouse breast cancer mod

158 cells, but not T47D control cells, developed lung metastasis in an ovarian hormone-independent manner

159 fectively reduced the number and size of the lung metastasis in both orthotopic xenograft and experim

160 eins involved in metabolic reprogramming and lung metastasis in breast cancer.

161 ost and/or the malignant cells also impaired lung metastasis in experimental mouse models.

162 lated in human prostate cancer and developed lung metastasis in immune-competent mice.

163 human melanoma tumor growth and experimental lung metastasis in mCXCR2(-/-) mice as compared with wil

164 CXCR4) and VEGF/VEGFR1 pathways in promoting lung metastasis in mice via BMDC recruitment using chime

165 e generation of tBregs and thereby abrogates lung metastasis in mice with established breast cancer.

166 genin suppressed murine melanoma B16F10 cell lung metastasis in mice, and inhibited cell migration an

167 erotopic and intravenous injection models of lung metastasis in mice, we found that IL5, a cytokine i

168 ion both in vitro and in vivo as well as the lung metastasis in mice, which could be rescued by ectop

169 es for immune cells, can efficiently inhibit lung metastasis in mice.

170 on of AP4 in CRC cells resulted in decreased lung metastasis in mice.

171 onal collagen I matrix, and tumor growth and lung metastasis in mice.

172 ces M2 macrophages and impedes breast cancer lung metastasis in mice.

173 nset of mammary tumorigenesis with increased lung metastasis in MMTV-Neu mouse model of spontaneous b

174 Here, we show that RhoGDI2 suppresses lung metastasis in mouse models by reducing the expressi

175 on and tumor invasion, and completely blocks lung metastasis in mouse models.

176 sistance to anoikis in vitro, and influenced lung metastasis in murine models.

177 PCA4248 inhibited the development of A375SM lung metastasis in nude mice.

178 lso impeded HCC cell migration and abolished lung metastasis in nude mice.

179 with intetumumab also significantly reduced lung metastasis in the A549 NSCLC xenograft model.

180 We found that platelets promote lung metastasis in the absence of NK cells in both acute

181 tion of endostatin dramatically inhibited OS lung metastasis in the p.104NN endostatin xenograft mode

182 ic PC3 xenograft tumor model and macroscopic lung metastasis in the rat Dunning AT3.1 prostate tumor

183 6BIO strongly reduced formation of lung metastasis in the well-established 4T1 mouse model

184 not decrease tumor growth, angiogenesis, or lung metastasis in these mice.

185 events progression to invasive carcinoma and lung metastasis in TRAMP mice.

186 viable circulating tumor cells and inhibited lung metastasis in two orthotopic models, but had little

187 -205 significantly inhibits the incidence of lung metastasis in vivo in a mouse tail vein model.

188 gration in vitro and intrahepatic and distal lung metastasis in vivo of HCC cells.

189 VEGFA increases lung metastasis in vivo, and this is abrogated by miR-45

190 eatment with a ROCK inhibitor reduced UMUC-3 lung metastasis in vivo, phenocopying the effect of Cav-

191 ell motility, intravasation, and spontaneous lung metastasis in vivo.

192 ed primary tumor growth, and greatly reduced lung metastasis in vivo.

193 ses cell migration and invasion in vitro and lung metastasis in vivo.

194 er cell line increased invasion in vitro and lung metastasis in vivo.

195 ent cancer phenotypes in vitro and growth of lung metastasis in vivo.

196 n in vitro and tumor growth and incidence of lung metastasis in vivo.

197 ed to significant inhibition of experimental lung metastasis in vivo.

198 hich specifically lack PMo, showed increased lung metastasis in vivo.

199 decreased CRC cell invasiveness in vitro and lung metastasis in vivo.

200 agar colony formation, and in vivo promoted lung metastasis independent of tumor growth.

201 tastatic seeding in an experimental model of lung metastasis, indicating that hypoxia-induced CAT enh

202 atic breast cancer (4T1) model, we show that lung metastasis is a feature of only a proportion of the

203 The patient who underwent RFA for a solitary lung metastasis is free of disease at the treatment site

204 del, the role of GOF mutant p53 in promoting lung metastasis is shown to be critically dependent on t

205 Lung metastasis is the lethal determinant in many cancer

206 d in a more invasive phenotype and increased lung metastasis likely due to an increase in Hedgehog si

207 sis that the endothelin axis is important in lung metastasis, lung metastatic bladder carcinoma cells

208 pathway components (REHB and RAPTOR) and of lung metastasis mediators (FSCN1 and SPARC).

209 e to the parental primary breast tumors, the lung metastasis (met)-derived mammary tumors exhibited a

210 reviously noted effects of blood clotting on lung metastasis might be mediated in part by a fibronect

211 t cancer metastasis in both the experimental lung metastasis model and the syngeneic mouse model.

212 In an experimental lung metastasis model established by tail vein injection

213 d metastatic foci development in a tail vein lung metastasis model in mice.

214 In the tumorigenesis and lung metastasis model in syngeneic mice, depletion of LK

215 ere sufficient to limit tumor formation in a lung metastasis model indicating that the NK cell popula

216 By employing a lung metastasis model of a murine breast cancer, we show

217 Employing a lung metastasis model of murine breast cancer, we found

218 The lung metastasis model was established by intravenous inj

219 When tested in a mouse melanoma lung metastasis model, the HSC-engineered iNKT cells eff

220 Using an ovalbumin-transfected B16 lung metastasis model, we show that heightened numbers o

221 Here, in an experimental mouse lung metastasis model, we showed that ATV generated eith

222 ay enhanced antitumor immunity in a melanoma lung metastasis model.

223 ent, mouse lung organ culture and an in vivo lung metastasis model.

224 ecreased tumor formation in the experimental lung metastasis model.

225 In this study, we used a murine melanoma lung-metastasis model and tested the therapeutic effects

226 cer cell lines and an in vivo bladder-cancer lung-metastasis model, and we successfully used these to

227 nistic anti-CD40 antibody (FGK4.5) in murine lung metastasis models involving CT26 and MC38, which ar

228 This was carried out in two lung metastasis models representative of high and low tu

229 nd pharmacologic blockade of ET receptors in lung metastasis models, we found that tumor ET-1 express

230 tumor growth in both B16F10 subcutaneous and lung metastasis models.

231 arker switch system in spontaneous breast-to-lung metastasis models.

232 ated lung cancer metastasis in an orthotopic lung metastasis mouse model.

233 n-regulates NPRA expression, also suppressed lung metastasis of A549 cells in nude mice and tumorigen

234 ibition of the subcutaneous tumor growth and lung metastasis of A549 cells in THC-treated animals as

235 TGFbeta promotes the lung metastasis of basal-like (but not the luminal-like)

236 s, Nidogen 1 (NID1) was confirmed to promote lung metastasis of breast cancer and melanoma, and its e

237 s, cell migration and invasion in vitro, and lung metastasis of breast cancer cells in vivo.

238 nd effective treatment for the prevention of lung metastasis of breast cancer patients.

239 ptional program in TAMs that acts to promote lung metastasis of breast tumors.

240 Similarly, experimental lung metastasis of E(2)-nonresponsive 4T1 mammary carcin

241 sible for fucosylated carbohydrate-dependent lung metastasis of epithelial cancers.

242 OS cells into mice, both molecules inhibited lung metastasis of ezrin-sensitive cells, but not ezrin-

243 essible compounds nearly completely inhibits lung metastasis of highly metastatic mammary carcinoma c

244 pic tumor model revealed an ET axis-mediated lung metastasis of macrophage-stimulated breast cancer c

245 ibition of the two-pore channel TPC2 reduced lung metastasis of mammary mouse cancer cells.

246 KLF8 knockdown inhibited the lung metastasis of MDA-MB-231 cells in nude mice.

247 ed metastatic tumor models, including B16OVA lung metastasis of melanoma and MC38 colon cancer liver

248 elective A2AR deletion significantly reduces lung metastasis of melanomas that express luciferase (fo

249 further derivatization significantly reduced lung metastasis of mice endovenously challenged with B16

250 r growth, peritoneal dissemination and liver/lung metastasis of orthotopically implanted PanC-1-luc c

251 RNA interference abrogates tumor growth and lung metastasis of otherwise highly invasive MDA-MB-231

252 ignaling by Gleevec inhibited the growth and lung metastasis of SN12-C cells grown orthotopically in

253 ent growth, cell migration, and experimental lung metastasis of T24 or UMUC3 human bladder cancer cel

254 cer cells significantly enhanced spontaneous lung metastasis of these cells without affecting primary

255 ha9beta1 were determined to be essential for lung metastasis of tumor cells.

256 gene signature was strongly associated with lung metastasis only in TNBC (P < 0.0001, Hazard ratio (

257 nts, elder patients were more likely to have lung metastasis (P < 0.001) and less likely to have only

258 owed strong anchorage-independent growth and lung metastasis potential in null mice.

259 EDICA treatment suppressed tumor growth, and lung metastasis, promoting a differentiated phenotype wh

260 Among the novel candidate lung metastasis proteins, Nidogen 1 (NID1) was confirmed

261 or cell survival, microvascular density, and lung metastasis relative to tumor-bearing littermate con

262 Lung metastasis required CCR4(+) regulatory T cells (Tre

263 that survived for more than 24 days without lung metastasis (responder group, n=5) or those that sur

264 The cancer-specific lung metastasis secretome signatures (LMSSs) displayed s

265 sion of a significant number of genes in the lung metastasis signature, but only activates a few bone

266 , and 1 patient underwent RFA for a solitary lung metastasis (size, 27 mm).

267 ution in cells without expression results in lung metastasis suppression.

268 suggesting that NMU might be a target of the lung metastasis suppressor effect of RhoGDI2.

269 In an established model of lung metastasis, systemic blockade by injection of a RAG

270 hangiogenesis and lymph node and spontaneous lung metastasis than Cl66-control tumors.

271 fects on tumor vascular density, growth, and lung metastasis than inhibition of VEGFR1 alone.

272 ted AIB1(-/-)/PyMT tumors also had much less lung metastasis than the recipient mice with transplante

273 DOX-MDSC promote breast tumor lung metastasis through MDSC miR-126a(+) exosomal-mediat

274 e of caveolin-1 in mammary tumorigenesis and lung metastasis using a molecular genetic approach.

275 iac injection model of experimental bone and lung metastasis using human breast carcinoma MDA-MB-435-

276 Experimental and spontaneous lung metastasis using murine tumor cells, without E-sele

277 f an adoptive transfer model of experimental lung metastasis using tumor-specific CTL as a relevant i

278 Melanoma lung metastasis was also decreased in the absence of IL1

279 The progressive impairment of lung metastasis was also observed with each successive m

280 combined immunodeficient mice, clonality of lung metastasis was dependent on cell number.

281 Furthermore, tumor growth and experimental lung metastasis was significantly decreased after expres

282 sively profile secreted proteins involved in lung metastasis, we applied quantitative mass spectromet

283 em were of relevance to human bladder cancer lung metastasis, we evaluated gene expression profiles o

284 tumor cells and the frequency and extent of lung metastasis were drastically reduced in SRC-1(-/-)/P

285 Here we showed that tumor growth and lung metastasis were enhanced in IL-17-deficient mice, a

286 Remarkably, s.c. tumor volume and lung metastasis were increased 2-fold in B cell-depleted

287 Here, mammary tumorigenesis and lung metastasis were investigated in wild-type (WT) and

288 In vivo, tumor growth and lung metastasis were promoted by transfection and overex

289 e observed decreased expression of HEXIM1 in lung metastasis when compared with primary mammary tumor

290 kdown dramatically inhibits tumor growth and lung metastasis, whereas ectopic expression of S1PR3 pro

291 ence for overexpressed CTSL as a promoter of lung metastasis, whereas high CTSL levels are maintained

292 n mammary tumor cells dramatically decreased lung metastasis, whereas LOXL2 overexpression promoted m

293 a6beta4 and alpha6beta1 were associated with lung metastasis, while exosomal integrin alphavbeta5 was

294 oral ginsenoside Ro significantly prevented lung metastasis with downregulation of integrin alphavbe

295 breast cancer can enhance intravasation and lung metastasis with no effect on primary tumor growth o

296 cells promoted uPA production and mammary to lung metastasis within 7 days.

297 or cell extravasation and melanoma dermal to lung metastasis without affecting primary tumor growth.

298 MMP downregulation in cancer cells decreased lung metastasis without affecting primary tumor growth.

299 ut not in tumor epithelial cells, attenuates lung metastasis without affecting primary tumor growth.

300 mammary tumor cells significantly diminishes lung metastasis without affecting tumor volume, invasion

301 A1 acts as a mandatory modifier of breast-to-lung metastasis without effects on primary tumor formati