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1 class of therapeutic agents for controlling cancer metastasis.
2 ion of mTORC1 in myeloid cells promoted lung cancer metastasis.
3 s that miRNA silencing might suppress breast cancer metastasis.
4 rtments is critical in understanding ovarian cancer metastasis.
5 g tumor progression, therapy resistance, and cancer metastasis.
6 of TAMs, leading to the suppression of lung cancer metastasis.
7 t clues for a better understanding of breast cancer metastasis.
8 a role in cancer related inflammation and/or cancer metastasis.
9 fective therapeutic strategy to prevent lung cancer metastasis.
10 cell types such as the study of hematogenous cancer metastasis.
11 druggable therapeutic targets that may limit cancer metastasis.
12 des a new therapeutic strategy to treat lung cancer metastasis.
13 ena such as wound healing, angiogenesis, and cancer metastasis.
14 ng development, pathogenic transmission, and cancer metastasis.
15 cruit repair cells to wound sites or inhibit cancer metastasis.
16 y partially explain how E2F1 promotes breast cancer metastasis.
17 erns greatly contribute to cell invasion and cancer metastasis.
18 of diseases including muscular dystrophy and cancer metastasis.
19 mitigate challenges associated with treating cancer metastasis.
20 icroenvironment that exert potent effects on cancer metastasis.
21 strated that miR-194 is a driver of prostate cancer metastasis.
22 JAM-C can be potentially targeted to control cancer metastasis.
23 irculating tumor cells (CTC) during prostate cancer metastasis.
24 is important in both normal development and cancer metastasis.
25 arkin to ubiquitinate HIF-1alpha and inhibit cancer metastasis.
26 ic role and new function for LOXL2 in breast cancer metastasis.
27 ological process that has been implicated in cancer metastasis.
28 biofilms, embryogenesis, wound healing, and cancer metastasis.
29 nstance,, changes in tRNA amounts facilitate cancer metastasis.
30 crease in motility, a feature reminiscent of cancer metastasis.
31 that are well known to be related to breast cancer metastasis.
32 ive CNAs that could be the driving events in cancer metastasis.
33 embrane, thereby having an essential role in cancer metastasis.
34 les of CXCR4 and CXCR2 signalings in gastric cancer metastasis.
35 lly targetable effector of CD109-driven lung cancer metastasis.
36 CXCR2 is more effective in reducing gastric cancer metastasis.
37 migration is essential for wound healing and cancer metastasis.
38 ocess involved in inflammatory responses and cancer metastasis.
39 e of Cad-11 in PSC activation and pancreatic cancer metastasis.
40 tified STAT4 as a critical player in ovarian cancer metastasis.
41 ic agent-a stressor-to immune modulation and cancer metastasis.
42 lmonary fibrosis and collagen-dependent lung cancer metastasis.
43 l function in a preclinical model of ovarian cancer metastasis.
44 tic interventions in the treatment of breast cancer metastasis.
45 t for normal development, wound healing, and cancer metastasis.
46 epithelial-mesenchymal transition and breast cancer metastasis.
47 egion leads to tumor initiation and prostate cancer metastasis.
48 al for development that can promote prostate cancer metastasis.
49 amics and functions of EMT plasticity during cancer metastasis.
50 (MMP) cleavage, leading to the inhibition of cancer metastasis.
51 of TGFbeta signaling able to suppress colon cancer metastasis.
52 g and estrogen responses and promotes breast cancer metastasis.
53 n cancer cells and macrophages during breast cancer metastasis.
54 otential medical application for controlling cancer metastasis.
55 in the effect of hyperinsulinemia on breast cancer metastasis.
56 sphorylation events mediate PDHc function in cancer metastasis.
57 ool for studying invasion, a crucial step in cancer metastasis.
58 ction and to prevent aberrant behavior as in cancer metastasis.
59 cers and is thought to play a role in breast cancer metastasis.
60 cs and cell migration and has been linked to cancer metastasis.
61 canonical Wnt signaling in organogenesis and cancer metastasis.
62 the study of cancer cell mechanosensing and cancer metastasis.
63 licated in normal cell cycle progression and cancer metastasis.
64 for specific metabolic targeting of ovarian cancer metastasis.
65 Liver is one of the most common sites of cancer metastasis.
66 and potential therapeutic target in bladder cancer metastasis.
67 duce metastases in a mouse model of prostate cancer metastasis.
68 cell spreading, microbial pathogenesis, and cancer metastasis.
69 yonic development that is also implicated in cancer metastasis.
70 ting integrins and integrin-dependent breast cancer metastasis.
71 evidence demonstrates that platelets support cancer metastasis.
72 molecular events modulating cell adhesion in cancer metastasis.
73 GluUUC and tRNAArgCCG as promoters of breast cancer metastasis.
74 as a robust suppressor of multiorgan breast cancer metastasis.
75 isition of drug resistance and in increasing cancer metastasis.
76 ial growth factor (VEGF), is responsible for cancer metastasis.
77 t of the metal-based nanomedicines to reduce cancer metastasis.
78 ons in vivo during embryonic development and cancer metastasis.
79 g and the investigation of the mechanisms of cancer metastasis.
80 logical and pathological processes including cancer metastasis.
81 but can also contribute to pathology such as cancer metastasis.
82 l during confined migration and thus promote cancer metastasis.
83 MP9) signalling as a driver for primary bone cancer metastasis.
84 lay important roles in organ development and cancer metastasis.
85 nd proliferation thus play critical roles in cancer metastasis.
86 ological processes such as morphogenesis and cancer metastasis.
87 of syngeneic mice, a frequent site of breast cancer metastasis.
88 that SET9 plays a role in modulating breast cancer metastasis.
89 on and invasion, suggesting a role in breast cancer metastasis.
90 t reverses EMT phenotypes suppressing breast cancer metastasis.
91 ormal omentum, the preferred site of ovarian cancer metastasis.
92 lication for Ambrisentan in the treatment of cancer metastasis.
93 reported to negatively correlate with breast cancer metastasis.
94 Lungs are one of the main sites of breast cancer metastasis.
95 ryonic development, tissue regeneration, and cancer metastasis.
96 ypoxia-induced tumor angiogenesis and breast cancer metastasis.
97 key cellular structures required for breast cancer metastasis.
98 phenotypes is sufficient to suppress breast cancer metastasis.
99 ng strategy to suppress postoperative breast cancer metastasis.
100 d as a potential nanomedicine against breast cancer metastasis.
101 administered agent to target CTCs and reduce cancer metastasis.
102 egulatory factor that impedes EMT and breast cancer metastasis.
103 relationship between EGFR and HUNK in breast cancer metastasis.
104 unication with tumor cells to promote breast cancer metastasis.
105 ole in development, tissue regeneration, and cancer metastasis.
106 , we elucidated the role of Wnt5a in ovarian cancer metastasis.
107 ays many critical roles in tumorigenesis and cancer metastasis.
108 onal development, immune cell migration, and cancer metastasis.
109 ogical processes like tissue development and cancer metastasis.
110 neural patterning, pathogen eradication, and cancer metastasis.
111 lial-mesenchymal transition (EMT) and breast cancer metastasis.
112 -suppressor microRNA with known functions in cancer metastasis.
113 rcome T-DM1-resistant disease and to prevent cancer metastasis.
114 identification of behaviors associated with cancer metastasis.
115 ion steps important for both development and cancer metastasis.
116 e cells and limit their effects on promoting cancer metastasis.
120 47.6%, 93.9%, 55.6%, and 91.9% for cervical cancer metastasis and 66.7%, 93.9%, 59.3%, and 95.5% for
121 SCs) or CSC-like cells play crucial roles in cancer metastasis and are exceptionally tolerant with ge
122 om cell differentiation and embryogenesis to cancer metastasis and biomaterial-tissue interactions.
124 nding to CLEC-2 and facilitates hematogenous cancer metastasis and cancer-associated thrombosis.
127 vering novel mechanisms of mutant p53-driven cancer metastasis and developing innovative therapeutics
128 general overview of how autophagy modulates cancer metastasis and discuss the significance of new fi
129 bited cell migration that closely related to cancer metastasis and displayed remarkable anti-tumor ef
132 cell line selection in the context of breast cancer metastasis and highlights the potential of organo
133 osed to be the initial event associated with cancer metastasis and how it occurred is still a mystery
134 ey transcription factors involved in ovarian cancer metastasis and identified STAT4 as a critical pla
135 blasts in mouse models of spontaneous breast cancer metastasis and in patients with breast cancer wit
137 ows an innovative strategy to block prostate cancer metastasis and invasion in the muscle through gen
138 high A2BR on mouse and human tumors promotes cancer metastasis and is an ideal candidate for therapeu
139 program that is reactivated during prostate cancer metastasis and is therapeutically targetable.
140 dly contribute to the development of ovarian cancer metastasis and metastatic tropism for the omentum
141 ehavior resembles the seed-and-soil model of cancer metastasis and offers a new model to understand f
142 eprogramming of glutaminolysis mediates lung cancer metastasis and offers a therapeutic strategy for
146 an important regulatory mechanism of breast cancer metastasis and provides a rationale for potential
148 r a novel role of dietary fats in colorectal cancer metastasis and reveal novel mechanisms underlying
151 ted role for host-expressed Wnt5a in ovarian cancer metastasis and suggest Fgr as a novel target for
152 tion of kinesin-1 motor functions and breast cancer metastasis and suggest PLD2 as a potential therap
153 e role of anesthetics used during surgery in cancer metastasis and the underlying mechanism remains l
155 tenascin C (TNC), an established promoter of cancer metastasis, and an EWS/ETS-repressed target gene.
156 s Exo70 as a substrate of ULK1 that inhibits cancer metastasis, and demonstrates that two counteracti
157 el, TMPRSS2 overexpression promoted prostate cancer metastasis, and HAI-2 overexpression efficiently
158 4, a prototypical CXC receptor and driver of cancer metastasis, and its endogenous ligand CXCL12.
159 during wound healing, organism development, cancer metastasis, and many other multicellular phenomen
162 g tumor cells for the prevention of prostate cancer metastasis, and potentially other cancers that sp
163 ates hypoxia-induced angiogenesis and breast cancer metastasis, and provides new insights into the fu
164 n of gene signatures associated with ovarian cancer metastasis, and reduced clonogenic cancer cell su
165 tasis, has therapeutic potential for ovarian cancer metastasis, and regulatory mechanisms of cell mot
166 all extracellular vesicles accelerate breast cancer metastasis, and targeted inhibition of tumor-deri
167 hypothesis that Fgf13 is critical for breast cancer metastasis, and that upregulation of Fgf13 may pa
168 cell migration drives embryonic development, cancer metastasis, and tissue repair and regeneration.
171 hological processes, such as inflammation or cancer metastasis, are accompanied by an increased vascu
172 s a previously obtained signature for breast cancer metastasis as an example to illustrate the critic
173 tablish that endothelial CXCR7 limits breast cancer metastasis at multiple steps in the metastatic ca
175 al cell migration is an early step in breast cancer metastasis, Atox1 levels in tumor cells may be a
176 capable of detecting the breast and prostate cancer metastasis biomarker, parathyroid hormone-related
177 NK cells are highly efficient at preventing cancer metastasis but are infrequently found in the core
178 RhoGDI2 specifically suppresses bladder cancer metastasis but not primary tumor growth, which in
179 h microenvironment forms a niche for ovarian cancer metastasis, but the mechanisms driving this proce
180 play a predominant role in colon and breast cancer metastasis, but the underlying molecular mechanis
181 erfamily members are important in colorectal cancer metastasis, but their signaling effects and predi
182 ycle (tricarboxylic acid cycle) and promotes cancer metastasis by adapting cancer cells to metabolic
184 of MBIL at learning risk factors for breast cancer metastasis by comparing it to the BN learning alg
185 how that PPARdelta contributes to colorectal cancer metastasis by expanding the CSC population, indic
186 herapeutic concept, i.e., the suppression of cancer metastasis by inhibiting a crucial protein-protei
189 gs establish ASB13 as a suppressor of breast cancer metastasis by promoting degradation of SNAI2 and
190 east cancer cells and TRIM28 promotes breast cancer metastasis by stabilizing TWIST1 and subsequently
191 he lactate-Gpr132 axis as a driver of breast cancer metastasis by stimulating tumor-macrophage interp
192 that a PDOX model of highly aggressive colon-cancer metastasis can identify effective drug combinatio
193 on during normal development and invasion in cancer metastasis, cells are required to withstand sever
194 To examine the role of ceramide in ovarian cancer metastasis, ceramide liposomes were employed and
196 patients before the manifestation of breast-cancer metastasis contain fewer genetic abnormalities th
197 viduals as well as in cancer survivors; (ii) cancer metastasis could be an early dissemination event
198 We further applied the methods to a breast cancer metastasis dataset, and discovered common early e
202 nonmetastatic, castration-resistant prostate cancer, metastasis-free survival was significantly longe
205 the gut microbiome as a new player in breast cancer metastasis; however, further studies are required
207 ation of pre-B-like cells in circulation and cancer metastasis, implying that the pre-B cell-TSLP axi
209 blish whether EVMM is an alternative form of cancer metastasis in addition to intravascular cancer di
211 Daxx also suppresses Slug-mediated lung cancer metastasis in an orthotopic lung metastasis mouse
215 vidence that LOXL2 is a key driver of breast cancer metastasis in two conditional transgenic mouse mo
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
223 eceptor 4 (CXCR4) plays an important role in cancer metastasis, in autoimmune diseases, and during st
224 Several key factors participate in breast cancer metastasis including long noncoding RNAs (lncRNAs
225 lpha5 integrin, does not suppress pancreatic cancer metastasis-indicating a role for RCP-dependent tr
233 meostatic and pathological processes such as cancer metastasis, its underlying mechanism and connecti
234 tumorigenesis and is required for pancreatic cancer metastasis, making it an excellent therapeutic ta
236 e development of an in vivo spontaneous lung cancer metastasis model, we show that the developmentall
237 ormed a large-scale study by creating breast cancer metastasis network and equipped it with different
238 nding of important biological processes like cancer metastasis, neuronal network development and woun
240 vivo, in both pathological processes such as cancer metastasis or physiological events such as immune
243 ibute to an improved understanding of breast cancer metastasis, providing new evidence in support of
244 lates cancer cell migration and invasion and cancer metastasis, recapitulating the effect of Twist.
245 c inhibition could be therapeutic for breast cancer metastasis regardless of primary tumor origin.
251 s of pre- and post-EMT tumor cells in breast cancer metastasis.See related commentary by Bunz, p.
252 study, results of two mouse models of breast cancer metastasis showed that ectopic expression of TGLI
253 is, and migration; nevertheless, its role in cancer metastasis, specifically via EMT, is not establis
257 roles of cell motility and proliferation in cancer metastasis, the device accurately predicts the me
258 Considering the distinct biology of ovarian cancer metastasis, the elucidation of the cellular and m
259 s and survival; however, its role in gastric cancer metastasis, the major cause of patient death, rem
260 nd closure also drive tissue development and cancer metastasis; therefore, embryonic wound repair has
261 cells to endothelial cells is a key step in cancer metastasis; therefore, identifying the key molecu
262 n endogenous Src inhibitor that can suppress cancer metastasis through complex interacting mechanisms
263 nocytes have been shown to play key roles in cancer metastasis through promotion of tumor cell extrav
265 -transcriptional network that governs breast cancer metastasis through RNA-binding protein-mediated t
268 investigating human primary bone tumors and cancer metastasis to the bone rely on the injection of h
269 evious studies revealed parameters of breast cancer metastasis to the brain, but its preference for t
270 r the first time, that TGLI1 mediates breast cancer metastasis to the brain, in part, through promoti
273 Here, we report that GALNT14 promotes breast cancer metastasis to the lung by enhancing the initiatio
277 n the bone endosteum that accompany prostate cancer metastasis to trabecular bone, with potential imp
279 ycolysis in tumors have been associated with cancer metastasis, tumor recurrence, and poor outcomes.
280 MBIL to learn risk factors for 5 year breast cancer metastasis using a clinical dataset we curated.
281 54.8%, 97.7%, 79.3%, and 93.1% for cervical cancer metastasis versus 64.6%, 98.6%, 86.1%, and 95.4%
283 e, we generated an in vivo model of prostate cancer metastasis via depletion of alpha3beta1 integrin,
284 iating potential and is involved in prostate cancer metastasis via direct regulation of CD44, a ubiqu
286 uthors show that cholesterol promotes breast cancer metastasis via its metabolite 27-hydroxycholester
287 that Aurora B induces EMT to promote breast cancer metastasis via OCT4/AKT/GSK3beta/Snail1 signaling
288 ablished a model that STAT4 promotes ovarian cancer metastasis via tumor-derived Wnt7a-induced activa
290 a proof-of-concept application for studying cancer metastasis, we applied this technique to measure
291 r to better understand the process of breast cancer metastasis, we have generated a mammary epithelia
294 risk factors that directly influence breast cancer metastasis, which can be investigated further.
295 a novel role of Ate1 in suppressing prostate cancer metastasis, which has a profound significance for
296 egun to explore the function of autophagy in cancer metastasis, which is of particular interest given
297 l process implicated in the initial stage of cancer metastasis, which is the major cause of tumor rec
298 n is one of the predominant sites for breast cancer metastasis, why breast cancer cells often become
300 ell invasion and promotes spontaneous breast cancer metastasis, without significantly affecting gene