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1 reased tumor growth and weight and inhibited lung metastasis.
2 melanomas have a similar ability to suppress lung metastasis.
3 as an energy reservoir to fuel breast cancer lung metastasis.
4 ation and in vivo xenograft tumor growth and lung metastasis.
5 el, results in increased tumor formation and lung metastasis.
6 pair of primary renal cell carcinoma and its lung metastasis.
7 d Akt2(-/-) mice display a high incidence of lung metastasis.
8 , ultimately attenuating melanoma growth and lung metastasis.
9 ial, tumor-endothelial cell interaction, and lung metastasis.
10 ecific Wnt5A knockdown also led to decreased lung metastasis.
11 kdown in transplanted NSCLC cells attenuated lung metastasis.
12 when tested in a mouse model of experimental lung metastasis.
13 rongly promoted both tumor cell invasion and lung metastasis.
14 eading to melanoma growth, angiogenesis, and lung metastasis.
15 ndothelial retraction required for efficient lung metastasis.
16  and MMP3 promoted melanoma tumor growth and lung metastasis.
17  of HCC cells along with tumor formation and lung metastasis.
18 bited significantly reduced tumor growth and lung metastasis.
19 ed suppression of ERK signaling and promotes lung metastasis.
20 Aqp7 caused reduced primary tumor burden and lung metastasis.
21 tors that sustain CIC phenotypes and promote lung metastasis.
22 ransition and promotes tumor progression and lung metastasis.
23 a decreased capacity for tumor formation and lung metastasis.
24 47 in tumor growth and their requirement for lung metastasis.
25 ft model and clinical data validated IL-8 in lung metastasis.
26 tected Tsp-1 from degradation and suppressed lung metastasis.
27 n axis under certain conditions) and in vivo lung metastasis.
28 Myc, the effect was markedly pronounced with lung metastasis.
29  endostatin did not significantly inhibit OS lung metastasis.
30  MMTV-PyMT mammary tumor cell lines enhances lung metastasis.
31 /E47-mediated modulation of tumor growth and lung metastasis.
32 and greatly increased the size and number of lung metastasis.
33 fer therapeutic benefits to prevent or treat lung metastasis.
34 reased migration/invasion, tumor growth, and lung metastasis.
35  displayed resistance to DEN-induced HCC and lung metastasis.
36 r growth, reduced vascularity, and decreased lung metastasis.
37 ier than PyMT mice, with increased lymph and lung metastasis.
38 expression in control tumor cells suppressed lung metastasis.
39  of breast tumors and further restrict their lung metastasis.
40 educed growth of primary tumors but enhanced lung metastasis.
41 s able to induce a marginal reduction of B16 lung metastasis.
42  or V2 with GIT1 further enhanced growth and lung metastasis.
43 al transition as well as fibrin invasion and lung metastasis.
44 ased the occurrence of vascular invasion and lung metastasis.
45  epithelial-mesenchymal transition (EMT) and lung metastasis.
46 l recurrence, peritoneal carcinomatosis, and lung metastasis.
47  which encode proteins that are required for lung metastasis.
48 rowth, macrophage residency/polarisation and lung metastasis.
49  the formation of highly malignant HCCs with lung metastasis.
50 e, and when injected into tail veins, led to lung metastasis.
51 ic vessel invasion (LVI), and lymph node and lung metastasis.
52 t cancer and found that it strongly promotes lung metastasis.
53 itiation, growth, latency, multiplicity, and lung metastasis.
54 t completely abrogate cancer progression and lung metastasis.
55 f mice with soluble JAM-C prevented melanoma lung metastasis.
56 as in metastatic melanoma including melanoma lung metastasis.
57 tarded MDA-MB-435 tumor growth and inhibited lung metastasis.
58 or anti-Bv8 antibodies significantly reduced lung metastasis.
59 erived cells (BMDCs) play a critical role in lung metastasis.
60 ure in the premetastatic lung and diminishes lung metastasis.
61  inhibition of tumor growth and experimental lung metastasis.
62 effective treatment of breast cancer and its lung metastasis.
63 antly affect tumorigenicity and experimental lung metastasis.
64 ts, this event was significantly enriched in lung metastasis.
65 estored T cells, and significantly repressed lung metastasis.
66 us mouse mammary tumor growth and associated lung metastasis.
67  migration, wound healing, tumor growth, and lung metastasis.
68 stemic tumour suppression in mouse models of lung metastasis.
69 ablishing a hospitable inflammatory niche in lung metastasis.
70 destabilization of pulmonary vasculature and lung metastasis.
71 pressive environment promotes gastric cancer lung metastasis.
72 umor cell extravasation, and mouse models of lung metastasis.
73 on, while overexpression of ASB13 suppressed lung metastasis.
74  in mice model, and also remarkably inhibits lung metastasis.
75 ntly decreased tumor growth and incidence of lung metastasis.
76 n fiber size and tumor density and increased lung metastasis.
77 culating tumor cells (CTCs) to suppress TNBC lung metastasis.
78 LOD2), in sarcomas has resulted in increased lung metastasis.
79 GFRalpha-induced invasion, promoting in vivo lung metastasis.
80 , MMTV-PyMT, leads to a profound increase in lung metastasis.
81 tion as a therapeutic target for eliminating lung metastasis.
82 tic niche to facilitate the establishment of lung metastasis.
83 ciated macrophages in a preclinical model of lung metastasis.
84 y tumor formation, it drastically suppressed lung metastasis.
85 ecreased EZH2 protein expression, repressing lung metastasis.
86 asis and in patients with breast cancer with lung metastasis.
87 89 overexpression inhibited tumor growth and lung metastasis.
88 metastasis in an experimental mouse model of lung metastasis.
89 ft lower leg and foot, as well as a solitary lung metastasis (12 mm).
90  10 involved nodes indicated a small risk of lung metastasis [3%-4%; odds ratio (OR) 3-4], tumors gre
91 c effects were found in both orthotropic and lung metastasis 4T1 breast cancer mice models.
92 nty-two patients (10.1%) were diagnosed with lung metastasis, 58 patients (8.1%) with liver metastasi
93 ypoxia in promoting primary tumor growth and lung metastasis, a 45-gene hypoxia response signature ef
94 from the radial growth phase (WM35) and from lung metastasis (A375-P).
95  miR-182 considerably increased, the rate of lung metastasis after amputation of the tumor-bearing li
96                One patient was found to have lung metastasis after HIFU and had an operation to remov
97 hy-1 showed markedly diminished experimental lung metastasis after injection of B16/F10 melanoma cell
98 mice showed markedly diminished experimental lung metastasis after injection of Lewis lung carcinoma
99 t reduction in tumor growth and experimental lung metastasis after PAR-1 silencing via systemic deliv
100 the sucrose was responsible for facilitating lung metastasis and 12-HETE production in breast tumors.
101  as platelet-derived P-selectin in promoting lung metastasis and also plays an important role in live
102                      FASN silencing enhanced lung metastasis and death in vivo.
103 eased tumor growth, reduced the incidence of lung metastasis and increased overall survival of mice w
104 ignificantly elevated expression of ALDH1 in lung metastasis and MDR1/LDH-A expression in liver metas
105   Ectopic expression of Zic1 suppressed both lung metastasis and peritoneal tumor dissemination of GC
106 in patient tumors (n=92), is associated with lung metastasis and poor overall survival of osteosarcom
107     High ezrin expression is associated with lung metastasis and poor survival in cancer.
108 of angiopoietin-2 in vascular remodeling and lung metastasis and provides new insights into mechanism
109 ng of IL33 in vivo resulted in inhibition of lung metastasis and significant attenuation of immune ce
110                  Treatment with DMH1 reduced lung metastasis and the tumors were less proliferative a
111 ed the number of cancer cells in xenografts, lung metastasis and then primary tumor growth was impair
112 ET-1 expression can serve as a biomarker for lung metastasis and whether it is required for metastati
113 atic carcinogenesis, haematogenous liver and lung metastasis, and cytomegalovirus infection.
114 b treatment, inhibited tumor growth, reduced lung metastasis, and improved survival.
115 d that MCPIP1 regulated ccRCC cell motility, lung metastasis, and mesenchymal phenotype by regulating
116 minent role of MTA2 in primary tumor growth, lung metastasis, and NF-kappaB signaling modulatory func
117 s antigens, inhibition of the progression of lung metastasis, and significantly extended animal survi
118 hylation as a potential molecular marker for lung metastasis, and suggest that epigenetic reversion o
119 cancer cells, biologic mechanisms regulating lung metastasis are not fully understood.
120                                         In a lung metastasis assay, NME1 overexpression failed to sig
121        We also noted a dramatic reduction in lung metastasis associated with decreased macrophage-med
122 nesis promotes both primary tumor growth and lung metastasis but is nonessential for bone metastasis.
123 ound to be organ specific, clearly enhancing lung metastasis but not affecting B16F1 liver metastasis
124 st cancer patients with low or high risks of lung metastasis, but not for bone metastasis.
125 n of either protein diminishes breast cancer lung metastasis, but the reason for this effect is uncle
126  clotting cascade is selectively involved in lung metastasis, but the reason for this selectivity is
127 cell line increased primary tumor growth and lung metastasis by 2.5- and 3-fold, respectively, when i
128 egs) play an essential role in breast cancer lung metastasis by inducing TGF-beta-dependent conversio
129 t-derived IL33 in facilitating breast cancer lung metastasis by modifying the immune microenvironment
130 oles in the regulation of breast cancer cell lung metastasis by modulating cell morphology and cell i
131 berberine treatment reduced tumor growth and lung metastasis by oral gavage, respectively.
132  a tumor suppressor in intestinal cancer and lung metastasis by triggering cancer cell death when net
133 integrin alphavbeta3 and fibronectin promote lung metastasis by upregulating Slug, defining a mechani
134 fter arrest in the lung, during experimental lung metastasis, by recruiting macrophages characterized
135 esponse against B16 melanoma and its distant lung metastasis compared with unmodified Grp170 and flag
136  metalloproteases eliminated degradation and lung metastasis, consistent with a direct link among inv
137                            The inhibition of lung metastasis correlated with reduced cancer cell migr
138 h ectopically CtBP expression show increased lung metastasis depending on the reduction of intracellu
139         Thus, transendothelial migration and lung metastasis development decreased by approximately 5
140 a cell extravasation in vitro and subsequent lung metastasis development in vivo.
141 this study showing that neutrophils regulate lung metastasis development through physical interaction
142 ressing the microRNA miR-200 does not affect lung metastasis development.
143 tastasis, (5) 1205Lu cells originated from a lung metastasis diagnosed in the same patient as WM793 c
144                             On the contrary, lung metastasis displayed ALDH+/CD133+ and MET-like phen
145 er of WT IMs increases the reduced number of lung metastasis foci in Ccl3 deficient mice.
146 or CCR1 in macrophages reduces the number of lung metastasis foci, as well as the number of MAMs accu
147 ress fibers, migration using Transwells, and lung metastasis following tail vein inoculation.
148  cells significantly contribute to recurrent lung metastasis formation after chemotherapy.
149 at deletion of RXR in myeloid cells enhances lung metastasis formation while not affecting primary tu
150 ice and, thereby, restoring immunity against lung metastasis formation.
151 ss by either route also dramatically reduced lung metastasis formation.
152  with ERalpha-negative breast cancers and in lung metastasis-free breast cancers.
153 methylation in circulating tumor DNA reduced lung metastasis-free survival.
154 tivate E-cadherin at the cell surface reduce lung metastasis from endogenous genetically driven tumor
155 nment promotes both primary lung tumours and lung metastasis from extrapulmonary neoplasms by contrib
156 tically reduced the incidence of spontaneous lung metastasis from primary tumors and decreased tumor
157  soluble isoforms conferred an advantage for lung metastasis from subcutaneous tumors (fs120/164 vs.
158 g therapeutic agent for early stage bone and lung metastasis from triple-negative breast cancer that
159                                 Single organ lung metastasis had longer median survival times compare
160             It was observed that cells after lung metastasis have the fastest migration and lowest st
161 TV-PyMT (PyMT), developed breast tumors with lung metastasis; however, mice deleted in p38delta (PyMT
162 ministration robustly inhibits breast cancer lung metastasis in a dose-dependent manner, associated w
163 mor cells in vitro but was found to increase lung metastasis in a mouse model of breast cancer metast
164 ung cancer cells and attenuates experimental lung metastasis in a xenograft mouse model.
165  we find that Lamellipodin depletion reduced lung metastasis in an orthotopic mouse breast cancer mod
166 eins involved in metabolic reprogramming and lung metastasis in breast cancer.
167 ost and/or the malignant cells also impaired lung metastasis in experimental mouse models.
168 lated in human prostate cancer and developed lung metastasis in immune-competent mice.
169 d EMT-like features, still formed tumors and lung metastasis in immune-deficient nude mice, but not i
170 CXCR4) and VEGF/VEGFR1 pathways in promoting lung metastasis in mice via BMDC recruitment using chime
171 e generation of tBregs and thereby abrogates lung metastasis in mice with established breast cancer.
172 genin suppressed murine melanoma B16F10 cell lung metastasis in mice, and inhibited cell migration an
173 erotopic and intravenous injection models of lung metastasis in mice, we found that IL5, a cytokine i
174 ion both in vitro and in vivo as well as the lung metastasis in mice, which could be rescued by ectop
175 ces M2 macrophages and impedes breast cancer lung metastasis in mice.
176 es for immune cells, can efficiently inhibit lung metastasis in mice.
177 on of AP4 in CRC cells resulted in decreased lung metastasis in mice.
178 d neutrophil lipid profiles and breast tumor lung metastasis in mice.
179 nset of mammary tumorigenesis with increased lung metastasis in MMTV-Neu mouse model of spontaneous b
180        Here, we show that RhoGDI2 suppresses lung metastasis in mouse models by reducing the expressi
181 on and tumor invasion, and completely blocks lung metastasis in mouse models.
182 bles complete inhibition of tumor growth and lung metastasis in mouse xenograft model, which is not p
183 sistance to anoikis in vitro, and influenced lung metastasis in murine models.
184 lso impeded HCC cell migration and abolished lung metastasis in nude mice.
185 ressive mammary tumor growth and spontaneous lung metastasis in orthotopic syngeneic TNBC mouse model
186  in combination with chemotherapy suppressed lung metastasis in spontaneous metastatic murine models.
187 ly restoring sphere formation, invasion, and lung metastasis in T24T(shATG7) cells.
188  with intetumumab also significantly reduced lung metastasis in the A549 NSCLC xenograft model.
189              We found that platelets promote lung metastasis in the absence of NK cells in both acute
190 Rs on primary tumour growth and experimental lung metastasis in the HT1080 xenograft model and highli
191 tion of endostatin dramatically inhibited OS lung metastasis in the p.104NN endostatin xenograft mode
192           6BIO strongly reduced formation of lung metastasis in the well-established 4T1 mouse model
193  not decrease tumor growth, angiogenesis, or lung metastasis in these mice.
194 viable circulating tumor cells and inhibited lung metastasis in two orthotopic models, but had little
195 -205 significantly inhibits the incidence of lung metastasis in vivo in a mouse tail vein model.
196  formation and invasion in vitro, as well as lung metastasis in vivo in human invasive BC cells.
197 gration in vitro and intrahepatic and distal lung metastasis in vivo of HCC cells.
198                              VEGFA increases lung metastasis in vivo, and this is abrogated by miR-45
199 eatment with a ROCK inhibitor reduced UMUC-3 lung metastasis in vivo, phenocopying the effect of Cav-
200 ent cancer phenotypes in vitro and growth of lung metastasis in vivo.
201 hich specifically lack PMo, showed increased lung metastasis in vivo.
202 decreased CRC cell invasiveness in vitro and lung metastasis in vivo.
203 ell motility, intravasation, and spontaneous lung metastasis in vivo.
204 ed primary tumor growth, and greatly reduced lung metastasis in vivo.
205 ses cell migration and invasion in vitro and lung metastasis in vivo.
206 er cell line increased invasion in vitro and lung metastasis in vivo.
207 lony formation, cell migration in vitro, and lung metastasis in vivo.
208 -derived cells to doxorubicin, and repressed lung metastasis in vivo.
209  agar colony formation, and in vivo promoted lung metastasis independent of tumor growth.
210 tastatic seeding in an experimental model of lung metastasis, indicating that hypoxia-induced CAT enh
211 del, the role of GOF mutant p53 in promoting lung metastasis is shown to be critically dependent on t
212                                              Lung metastasis is the lethal determinant in many cancer
213 PTGES/PGE(2) signaling in tumorigenicity and lung metastasis is through immunosuppression.
214 d in a more invasive phenotype and increased lung metastasis likely due to an increase in Hedgehog si
215                              In contrast, in lung metastasis (LuM), MDSC programming is driven mainly
216 dentifies stem cell populations that mediate lung metastasis, mechanisms underlying the role of this
217  pathway components (REHB and RAPTOR) and of lung metastasis mediators (FSCN1 and SPARC).
218 e to the parental primary breast tumors, the lung metastasis (met)-derived mammary tumors exhibited a
219 reviously noted effects of blood clotting on lung metastasis might be mediated in part by a fibronect
220 t cancer metastasis in both the experimental lung metastasis model and the syngeneic mouse model.
221 d metastatic foci development in a tail vein lung metastasis model in mice.
222                     In the tumorigenesis and lung metastasis model in syngeneic mice, depletion of LK
223 ere sufficient to limit tumor formation in a lung metastasis model indicating that the NK cell popula
224                               By employing a lung metastasis model of a murine breast cancer, we show
225                                  Employing a lung metastasis model of murine breast cancer, we found
226                                          The lung metastasis model was established by intravenous inj
227 ed in the lungs of Raptor KO mice in the LLC lung metastasis model, leading to decreased Th1 response
228              When tested in a mouse melanoma lung metastasis model, the HSC-engineered iNKT cells eff
229                           In an experimental lung metastasis model, the pharmacological depletion of
230                   In a spontaneous breast-to-lung metastasis model, we found that primary tumor cells
231 ay enhanced antitumor immunity in a melanoma lung metastasis model.
232 ent, mouse lung organ culture and an in vivo lung metastasis model.
233 ecreased tumor formation in the experimental lung metastasis model.
234     In this study, we used a murine melanoma lung-metastasis model and tested the therapeutic effects
235                  This was carried out in two lung metastasis models representative of high and low tu
236 nd pharmacologic blockade of ET receptors in lung metastasis models, we found that tumor ET-1 express
237 arker switch system in spontaneous breast-to-lung metastasis models.
238 tumor growth in both B16F10 subcutaneous and lung metastasis models.
239 ated lung cancer metastasis in an orthotopic lung metastasis mouse model.
240  subcutaneous growth of LLC1 and B16F10, and lung metastasis of B16F10 tumors.
241                         TGFbeta promotes the lung metastasis of basal-like (but not the luminal-like)
242 lator of the sphere formation, invasion, and lung metastasis of BCs, providing significant insight in
243                      Liver tumour growth and lung metastasis of breast and liver cancer cells are inh
244 s, Nidogen 1 (NID1) was confirmed to promote lung metastasis of breast cancer and melanoma, and its e
245 ted to simultaneously inhibit the growth and lung metastasis of breast cancer by delivering quercetin
246 s, cell migration and invasion in vitro, and lung metastasis of breast cancer cells in vivo.
247 ized drug delivery systems against malignant lung metastasis of breast cancer have been extensively s
248                                              Lung metastasis of breast cancer is a leading cause of c
249 ns are related to high aggressiveness in the lung metastasis of CRC.
250 OS cells into mice, both molecules inhibited lung metastasis of ezrin-sensitive cells, but not ezrin-
251  loss of DLL1 inhibits both tumor growth and lung metastasis of luminal breast cancer.
252 pic tumor model revealed an ET axis-mediated lung metastasis of macrophage-stimulated breast cancer c
253 ibition of the two-pore channel TPC2 reduced lung metastasis of mammary mouse cancer cells.
254 ed metastatic tumor models, including B16OVA lung metastasis of melanoma and MC38 colon cancer liver
255 elective A2AR deletion significantly reduces lung metastasis of melanomas that express luciferase (fo
256 further derivatization significantly reduced lung metastasis of mice endovenously challenged with B16
257                                              Lung metastasis of orthotopic BT474-TtzmR xenografts was
258 r growth, peritoneal dissemination and liver/lung metastasis of orthotopically implanted PanC-1-luc c
259 ts in mice resulted in a marked reduction of lung metastasis of podoplanin-expressing B16F10 cells.
260 ha9beta1 were determined to be essential for lung metastasis of tumor cells.
261  gene signature was strongly associated with lung metastasis only in TNBC (P < 0.0001, Hazard ratio (
262 nts, elder patients were more likely to have lung metastasis (P < 0.001) and less likely to have only
263 owed strong anchorage-independent growth and lung metastasis potential in null mice.
264 EDICA treatment suppressed tumor growth, and lung metastasis, promoting a differentiated phenotype wh
265                    Among the novel candidate lung metastasis proteins, Nidogen 1 (NID1) was confirmed
266 om vertical growth phase (VGP), and skin and lung metastasis, respectively.
267  that survived for more than 24 days without lung metastasis (responder group, n=5) or those that sur
268 n to VGP melanoma cells, cells from skin and lung metastasis reveal similar or significantly differen
269                          The cancer-specific lung metastasis secretome signatures (LMSSs) displayed s
270 sion of a significant number of genes in the lung metastasis signature, but only activates a few bone
271 hat knockout of CDK12 in an in vivo model of lung metastasis significantly decreased the ability of O
272                                              Lung metastasis sites developed after mice were exposed
273                                 We confirmed lung metastasis-specific increase in oxidative stress an
274                   In an established model of lung metastasis, systemic blockade by injection of a RAG
275 fects on tumor vascular density, growth, and lung metastasis than inhibition of VEGFR1 alone.
276 with sevoflurane leads to significantly more lung metastasis than with propofol in both syngeneic mur
277 have shown that aspirin dramatically reduced lung metastasis through inhibition of COX-1 while the ca
278                DOX-MDSC promote breast tumor lung metastasis through MDSC miR-126a(+) exosomal-mediat
279 vation in the lung has been shown to promote lung metastasis, tumor therapy will require approaches t
280                 Experimental and spontaneous lung metastasis using murine tumor cells, without E-sele
281 portantly, inhibition of neutrophil-mediated lung metastasis via the sustained release of Zileuton.
282 y difference observed for cells from VGP and lung metastasis was accompanied by the largest separatio
283                                     Melanoma lung metastasis was also decreased in the absence of IL1
284   Furthermore, tumor growth and experimental lung metastasis was significantly decreased after expres
285 sively profile secreted proteins involved in lung metastasis, we applied quantitative mass spectromet
286                     Using multiple models of lung metastasis, we show that interleukin (IL)-33-depend
287                   Larger tumors and enhanced lung metastasis were seen in S1pr1 ECKO, whereas S1pr1 E
288 e observed decreased expression of HEXIM1 in lung metastasis when compared with primary mammary tumor
289 kdown dramatically inhibits tumor growth and lung metastasis, whereas ectopic expression of S1PR3 pro
290 ence for overexpressed CTSL as a promoter of lung metastasis, whereas high CTSL levels are maintained
291 n mammary tumor cells dramatically decreased lung metastasis, whereas LOXL2 overexpression promoted m
292 In contrast, loss of any Akt isoform reduced lung metastasis while vascular invasion was reduced with
293 a6beta4 and alpha6beta1 were associated with lung metastasis, while exosomal integrin alphavbeta5 was
294          We focused on patients exhibiting 1 lung metastasis who underwent an AR (segmentectomy) or a
295 e review identified 79 cases of metachronous lung metastasis with a survival of 120.0 +/- 6.32 months
296  oral ginsenoside Ro significantly prevented lung metastasis with downregulation of integrin alphavbe
297 ut not in tumor epithelial cells, attenuates lung metastasis without affecting primary tumor growth.
298 or cell extravasation and melanoma dermal to lung metastasis without affecting primary tumor growth.
299 MMP downregulation in cancer cells decreased lung metastasis without affecting primary tumor growth.
300 A1 acts as a mandatory modifier of breast-to-lung metastasis without effects on primary tumor formati

 
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