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1 icroenvironment that exert potent effects on cancer metastasis.
2 strated that miR-194 is a driver of prostate cancer metastasis.
3 evidence demonstrates that platelets support cancer metastasis.
4 molecular events modulating cell adhesion in cancer metastasis.
5 GluUUC and tRNAArgCCG as promoters of breast cancer metastasis.
6 as a robust suppressor of multiorgan breast cancer metastasis.
7 isition of drug resistance and in increasing cancer metastasis.
8 ial growth factor (VEGF), is responsible for cancer metastasis.
9 ons in vivo during embryonic development and cancer metastasis.
10 g and the investigation of the mechanisms of cancer metastasis.
11 ic role and new function for LOXL2 in breast cancer metastasis.
12 logical and pathological processes including cancer metastasis.
13 but can also contribute to pathology such as cancer metastasis.
14 l during confined migration and thus promote cancer metastasis.
15 ological process that has been implicated in cancer metastasis.
16 lay important roles in organ development and cancer metastasis.
17 nd proliferation thus play critical roles in cancer metastasis.
18 ological processes such as morphogenesis and cancer metastasis.
19 of syngeneic mice, a frequent site of breast cancer metastasis.
20 that SET9 plays a role in modulating breast cancer metastasis.
21 a viable therapeutic opportunity to prevent cancer metastasis.
22 tential therapeutic target for inhibition of cancer metastasis.
23 t are able to reliably detect the process of cancer metastasis.
24 biofilms, embryogenesis, wound healing, and cancer metastasis.
25 ficant role for mRNA-edited Gabra3 in breast cancer metastasis.
26 action as a novel approach to inhibit breast cancer metastasis.
27 nexin 9 (SNX9) as a new regulator of breast cancer metastasis.
28 ancer pleural effusion and spontaneous colon cancer metastasis.
29 ignificant role of cholesterol metabolism in cancer metastasis.
30 grams within the lung that are permissive to cancer metastasis.
31 ved function, with important implications in cancer metastasis.
32 is for targeting MDSCs to reduce the risk of cancer metastasis.
33 rgan formation, immunological reactions, and cancer metastasis.
34 in the host microenvironment also suppresses cancer metastasis.
35 phorylated GIV at the FAs is enhanced during cancer metastasis.
36 nstance,, changes in tRNA amounts facilitate cancer metastasis.
37 tential as a drug target for limiting breast cancer metastasis.
38 planation for susceptibility of the lungs to cancer metastasis.
39 RC-2 as a prominent metabolic coordinator of cancer metastasis.
40 ation whose invasiveness has been likened to cancer metastasis.
41 crease in motility, a feature reminiscent of cancer metastasis.
42 on-the key signaling pathway associated with cancer metastasis.
43 ctly inactivate gene transcription and drive cancer metastasis.
44 e report that PIPKIgamma is vital for breast cancer metastasis.
45 es has implications for our understanding of cancer metastasis.
46 A family and has an important role in breast cancer metastasis.
47 methylation and might further contribute to cancer metastasis.
48 myocardial infarction, ischemic stroke, and cancer metastasis.
49 ovide a potential approach to suppression of cancer metastasis.
50 nd healing, and pathologic processes such as cancer metastasis.
51 ive CNAs that could be the driving events in cancer metastasis.
52 s are implicated in metabolic adaptation and cancer metastasis.
53 es for developing novel drugs for preventing cancer metastasis.
54 tissue development, epithelial stemness, and cancer metastasis.
55 bryonic development, adult tissue repair and cancer metastasis.
56 player in cell migration, cell invasion, and cancer metastasis.
57 2 and interleukin-6, cytokines implicated in cancer metastasis.
58 jects, and human cell line models of bladder cancer metastasis.
59 ediated pathway that is essential for breast cancer metastasis.
60 n in tumor tissues is associated with breast cancer metastasis.
61 embrane, thereby having an essential role in cancer metastasis.
62 e lung metastasis in a mouse model of breast cancer metastasis.
63 ies aimed at preventing and treating ovarian cancer metastasis.
64 t-based immunotherapies to prevent or reduce cancer metastasis.
65 hat could be responsible for Dsg3-associated cancer metastasis.
66 oting tumor neoangiogenesis and by enhancing cancer metastasis.
67 tomous role in early vs late steps of breast cancer metastasis.
68 croRNAs (miRs) can have an important role in cancer metastasis.
69 lar targets for the inhibition of pancreatic cancer metastasis.
70 ges in the tumor microenvironment facilitate cancer metastasis.
71 tiple cancer cell lines and murine models of cancer metastasis.
72 biologists to gain a better understanding of cancer metastasis.
73 s metastasis as an important mode of ovarian cancer metastasis.
74 stases offer a potentially powerful model of cancer metastasis.
75 member BMP4 is a potent suppressor of breast cancer metastasis.
76 ively during development, wound healing, and cancer metastasis.
77 de-repression of vinculin and regulate lung cancer metastasis.
78 tively regulated by RKIP and promotes breast cancer metastasis.
79 les of CXCR4 and CXCR2 signalings in gastric cancer metastasis.
80 s been suggested to play a causative role in cancer metastasis.
81 KS-related peptides in the treatment of lung cancer metastasis.
82 thus promoting both early and late steps of cancer metastasis.
83 lly targetable effector of CD109-driven lung cancer metastasis.
84 m of posttranslational regulation of EMT and cancer metastasis.
85 o serve as potential therapeutic targets for cancer metastasis.
86 ng as a therapeutic strategy to limit breast cancer metastasis.
87 NM2, miR-199a, and HIF, with implications in cancer metastasis.
88 2 deficiency has a protective effect against cancer metastasis.
89 r signaling pathway in the process of breast cancer metastasis.
90 JAM-C can be potentially targeted to control cancer metastasis.
91 CXCR2 is more effective in reducing gastric cancer metastasis.
92 ocess involved in inflammatory responses and cancer metastasis.
93 e of Cad-11 in PSC activation and pancreatic cancer metastasis.
94 tified STAT4 as a critical player in ovarian cancer metastasis.
95 ic agent-a stressor-to immune modulation and cancer metastasis.
96 lmonary fibrosis and collagen-dependent lung cancer metastasis.
97 tic interventions in the treatment of breast cancer metastasis.
98 t for normal development, wound healing, and cancer metastasis.
99 epithelial-mesenchymal transition and breast cancer metastasis.
100 egion leads to tumor initiation and prostate cancer metastasis.
101 irculating tumor cells (CTC) during prostate cancer metastasis.
102 al for development that can promote prostate cancer metastasis.
103 (MMP) cleavage, leading to the inhibition of cancer metastasis.
104 of TGFbeta signaling able to suppress colon cancer metastasis.
105 is important in both normal development and cancer metastasis.
106 g and estrogen responses and promotes breast cancer metastasis.
107 n cancer cells and macrophages during breast cancer metastasis.
108 otential medical application for controlling cancer metastasis.
109 in the effect of hyperinsulinemia on breast cancer metastasis.
110 ool for studying invasion, a crucial step in cancer metastasis.
111 ction and to prevent aberrant behavior as in cancer metastasis.
112 cs and cell migration and has been linked to cancer metastasis.
113 canonical Wnt signaling in organogenesis and cancer metastasis.
114 the study of cancer cell mechanosensing and cancer metastasis.
115 licated in normal cell cycle progression and cancer metastasis.
116 arkin to ubiquitinate HIF-1alpha and inhibit cancer metastasis.
117 Liver is one of the most common sites of cancer metastasis.
118 and potential therapeutic target in bladder cancer metastasis.
119 duce metastases in a mouse model of prostate cancer metastasis.
120 cell spreading, microbial pathogenesis, and cancer metastasis.
121 yonic development that is also implicated in cancer metastasis.
122 ting integrins and integrin-dependent breast cancer metastasis.
123 47.6%, 93.9%, 55.6%, and 91.9% for cervical cancer metastasis and 66.7%, 93.9%, 59.3%, and 95.5% for
124 coupled receptor (GPCR) implicated in breast cancer metastasis and an indicator of poor prognosis in
126 om cell differentiation and embryogenesis to cancer metastasis and biomaterial-tissue interactions.
129 bition during involution reduced the risk of cancer metastasis and correlated with decreased lymphang
130 IG1 is an independent risk factor for breast cancer metastasis and death in stage I/II patients.
132 general overview of how autophagy modulates cancer metastasis and discuss the significance of new fi
133 bited cell migration that closely related to cancer metastasis and displayed remarkable anti-tumor ef
135 he potential to further our understanding of cancer metastasis and enhance the care of cancer patient
136 ey transcription factors involved in ovarian cancer metastasis and identified STAT4 as a critical pla
138 lymphatic system plays an important role in cancer metastasis and inhibition of lymphangiogenesis co
139 high A2BR on mouse and human tumors promotes cancer metastasis and is an ideal candidate for therapeu
140 program that is reactivated during prostate cancer metastasis and is therapeutically targetable.
141 eprogramming of glutaminolysis mediates lung cancer metastasis and offers a therapeutic strategy for
144 ole in driving the development of colorectal cancer metastasis and present challenges and opportuniti
145 To further elucidate the role of CTCs in cancer metastasis and prognosis, effective methods for i
147 an important regulatory mechanism of breast cancer metastasis and provides a rationale for potential
150 the NFkappaB pathway contributes to prostate cancer metastasis and suggest FN14 as a candidate therap
151 tion of kinesin-1 motor functions and breast cancer metastasis and suggest PLD2 as a potential therap
152 er specimens that is closely correlated with cancer metastasis and that EphA2 promotes EMT of gastric
153 tenascin C (TNC), an established promoter of cancer metastasis, and an EWS/ETS-repressed target gene.
155 during wound healing, organism development, cancer metastasis, and many other multicellular phenomen
158 g tumor cells for the prevention of prostate cancer metastasis, and potentially other cancers that sp
159 etween inflammation and lymphangiogenesis in cancer metastasis, and propose therapeutic intervention
160 monstrate the involvement of Nanog in breast cancer metastasis, and provide the basis for the reporte
161 tasis, has therapeutic potential for ovarian cancer metastasis, and regulatory mechanisms of cell mot
163 biological processes including development, cancer metastasis, and wound healing, suggesting conditi
167 AAV) delivery significantly suppressed colon cancer metastasis, as did CKB inhibition with a small-mo
168 tablish that endothelial CXCR7 limits breast cancer metastasis at multiple steps in the metastatic ca
169 SNAIL1 has been suggested to regulate breast cancer metastasis based on analyses of human breast tumo
170 capable of detecting the breast and prostate cancer metastasis biomarker, parathyroid hormone-related
171 NK cells are highly efficient at preventing cancer metastasis but are infrequently found in the core
172 gration, a result with relevance not only to cancer metastasis but for 3D migration in other settings
173 RhoGDI2 specifically suppresses bladder cancer metastasis but not primary tumor growth, which in
174 lassical monocytes promote tumorigenesis and cancer metastasis, but how nonclassical "patrolling" mon
175 h microenvironment forms a niche for ovarian cancer metastasis, but the mechanisms driving this proce
176 erfamily members are important in colorectal cancer metastasis, but their signaling effects and predi
178 ribonucleoprotein M (hnRNPM) promotes breast cancer metastasis by activating the switch of alternativ
179 ortant role for DeltaNp63alpha in preventing cancer metastasis by inhibition of Erk2 signaling via MK
181 h protein with kazal motifs) controls breast cancer metastasis by modulating a novel, non-canonical a
182 We conclude that E6AP suppresses breast cancer metastasis by regulating actin cytoskeleton remod
183 east cancer cells and TRIM28 promotes breast cancer metastasis by stabilizing TWIST1 and subsequently
184 he lactate-Gpr132 axis as a driver of breast cancer metastasis by stimulating tumor-macrophage interp
187 To examine the role of ceramide in ovarian cancer metastasis, ceramide liposomes were employed and
189 e the possibility of using mifepristone as a cancer metastasis chemopreventive, we performed a system
191 ssay that models the initial step of ovarian cancer metastasis, clearance of the mesothelial cell lay
192 ly improve the prediction accuracy of breast cancer metastasis compared with several popular approach
193 patients before the manifestation of breast-cancer metastasis contain fewer genetic abnormalities th
194 viduals as well as in cancer survivors; (ii) cancer metastasis could be an early dissemination event
195 ertain biological networks underlying breast cancer metastasis differ in a proliferation-dependent ma
196 in cancer; exosome mediated communication in cancer metastasis, drug resistance, and interfacing with
197 Wnt11 in mouse early development and also in cancer metastasis, during which EMT plays a crucial role
203 blish whether EVMM is an alternative form of cancer metastasis in addition to intravascular cancer di
204 oliferation and overcome immune rejection of cancer metastasis in allogeneic mice through modulation
206 Daxx also suppresses Slug-mediated lung cancer metastasis in an orthotopic lung metastasis mouse
207 re, overexpression of EcSOD inhibited breast cancer metastasis in both the experimental lung metastas
209 ng C to T changes at a locus associated with cancer metastasis in breast cancer cell lines and serum-
211 ents TGFbeta-induced EMT and inhibits breast cancer metastasis in mice, whereas enforced expression o
215 vidence that LOXL2 is a key driver of breast cancer metastasis in two conditional transgenic mouse mo
216 p enhanced cell migration/invasion in vitro, cancer metastasis in vivo, and particularly the EMT char
217 e resistant to melanoma, prostate and breast cancer metastasis in vivo, and this was intrinsic to NK
218 mine the effects of miR-23b/-27b on prostate cancer metastasis in vivo, orthotopic prostate xenograft
224 lpha5 integrin, does not suppress pancreatic cancer metastasis-indicating a role for RCP-dependent tr
231 new strategies for the prevention of breast cancer metastasis is justifiably at the center of clinic
232 n and migration that occurs, for example, in cancer metastasis is rooted in the ability of cells to n
239 meostatic and pathological processes such as cancer metastasis, its underlying mechanism and connecti
240 tumorigenesis and is required for pancreatic cancer metastasis, making it an excellent therapeutic ta
242 the mechanism by which CXCR4 mediates breast cancer metastasis, MCF-7 breast carcinoma cells were tra
243 e development of an in vivo spontaneous lung cancer metastasis model, we show that the developmentall
244 ormed a large-scale study by creating breast cancer metastasis network and equipped it with different
245 nding of important biological processes like cancer metastasis, neuronal network development and woun
246 vivo, in both pathological processes such as cancer metastasis or physiological events such as immune
248 lates cancer cell migration and invasion and cancer metastasis, recapitulating the effect of Twist.
251 thelial-mesenchymal transitions (EMT) during cancer metastasis remains a major challenge in modern bi
254 rstanding the molecular and genetic basis of cancer, metastasis remains the cause of >90% of cancer-r
257 e MDSCs possess dual functions to facilitate cancer metastasis: suppress immune surveillance and stim
261 ntal support for a role for SNAIL1 in breast cancer metastasis that develops in an immunocompetent tu
262 aled a dynamic relationship between CAFs and cancer metastasis that has counter-intuitive ramificatio
263 we report a role for lncRNA BCAR4 in breast cancer metastasis that is mediated by chemokine-induced
265 implicated as a cell of origin for prostate cancer metastasis, the pathways that enable metastatic d
266 fusion has been suggested as a mechanism of cancer metastasis, the underlying mechanisms defining th
267 cells to endothelial cells is a key step in cancer metastasis; therefore, identifying the key molecu
268 at PNR could promote ERalpha-negative breast cancer metastasis through activation of IL-13Ralpha2-med
269 n endogenous Src inhibitor that can suppress cancer metastasis through complex interacting mechanisms
270 or-beta1 (TGF-beta1) play important roles in cancer metastasis through different mechanisms: TGF-beta
272 -transcriptional network that governs breast cancer metastasis through RNA-binding protein-mediated t
273 ntaneous mouse models of melanoma and breast cancer metastasis to demonstrate the efficacy and mechan
274 is study, we have employed a model of breast cancer metastasis to examine the mechanism by which IL-1
277 investigating human primary bone tumors and cancer metastasis to the bone rely on the injection of h
279 Here, we report that GALNT14 promotes breast cancer metastasis to the lung by enhancing the initiatio
283 el of breast cancer, we show that AM promote cancer metastasis to the lungs by suppressing antitumor
284 n the bone endosteum that accompany prostate cancer metastasis to trabecular bone, with potential imp
286 54.8%, 97.7%, 79.3%, and 93.1% for cervical cancer metastasis versus 64.6%, 98.6%, 86.1%, and 95.4%
287 e, we generated an in vivo model of prostate cancer metastasis via depletion of alpha3beta1 integrin,
288 iating potential and is involved in prostate cancer metastasis via direct regulation of CD44, a ubiqu
290 uthors show that cholesterol promotes breast cancer metastasis via its metabolite 27-hydroxycholester
291 ablished a model that STAT4 promotes ovarian cancer metastasis via tumor-derived Wnt7a-induced activa
293 r to better understand the process of breast cancer metastasis, we have generated a mammary epithelia
295 ve migration causing autoimmune diseases and cancer metastasis, whereas reduced capacity for migratio
296 esenchymal transition (EMT) is essential for cancer metastasis, which is a multistep complicated proc
297 egun to explore the function of autophagy in cancer metastasis, which is of particular interest given
298 n is one of the predominant sites for breast cancer metastasis, why breast cancer cells often become
299 3D extracellular matrix (ECM) is crucial to cancer metastasis, yet little is known of the molecular
300 nto capillaries is an early and key event in cancer metastasis, yet not all cancer cells are imbued w
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