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1 ly serves as a multivariate predictor of the metastatic phenotype ().
2 ses, including cancer stem cell survival and metastatic phenotype.
3 ay a specific role in the development of the metastatic phenotype.
4 romotes a transition to a more malignant and metastatic phenotype.
5 ding matrix, indicative of a transformed and metastatic phenotype.
6 n 4T1 cells conveys in vitro correlates of a metastatic phenotype.
7 vely lost as the cells take on a more highly metastatic phenotype.
8 s, promotes and contributes to IBC's extreme metastatic phenotype.
9 cells and the ECM molecule FN to promote the metastatic phenotype.
10 tegrin alphavbeta3 that is associated with a metastatic phenotype.
11 that loss of TBR2 leads to acquisition of a metastatic phenotype.
12 for further investigation in the context of metastatic phenotype.
13 differential gene expression regulating the metastatic phenotype.
14 nes differentially expressed with respect to metastatic phenotype.
15 was demonstrated between Fas expression and metastatic phenotype.
16 s can play important functional roles in the metastatic phenotype.
17 ression is the transition to an invasive and metastatic phenotype.
18 te angiogenesis are integral features of the metastatic phenotype.
19 thway contributes distinct properties to the metastatic phenotype.
20 ntially with Adriamycin and FUdR expressed a metastatic phenotype.
21 egulate hAR is, in part, responsible for the metastatic phenotype.
22 by facilitating growth or acquisition of the metastatic phenotype.
23 differentiation and partially reversing the metastatic phenotype.
24 have an influence on the development of the metastatic phenotype.
25 ich Met activity contributes to the invasive/metastatic phenotype.
26 ession that correlates with progression to a metastatic phenotype.
27 ole in the development and regulation of the metastatic phenotype.
28 sts that primary tissue is predictive of the metastatic phenotype.
29 and demonstrate their ability to induce the metastatic phenotype.
30 of FasL (95%), suggesting association with a metastatic phenotype.
31 velopment of melanoma and acquisition of the metastatic phenotype.
32 estrogen receptor (ER) negative, and highly metastatic phenotype.
33 oteases and angiogenic factors, and a highly metastatic phenotype.
34 aments alone is not sufficient to confer the metastatic phenotype.
35 with the progression of a primary tumor to a metastatic phenotype.
36 y to regulate an undifferentiated and highly metastatic phenotype.
37 re cell motility closely correlates with the metastatic phenotype.
38 and seem to be a feature of the aggressive, metastatic phenotype.
39 growth factor receptor)-positive, and highly metastatic phenotype.
40 actor SOX9, that promote proliferation and a metastatic phenotype.
41 umoral heterogeneity in the development of a metastatic phenotype.
42 Variable exon usage is associated with metastatic phenotype.
43 noma (HCC) fostering a highly aggressive and metastatic phenotype.
44 and diagnostic indicators of the aggressive, metastatic phenotype.
45 aling cascades that drive the MDA-9-mediated metastatic phenotype.
46 AC), a cancer type characterized by a highly metastatic phenotype.
47 but also cell signaling, which promotes the metastatic phenotype.
48 patient samples directly correlates with the metastatic phenotype.
49 sformed NIH 3T3 cells and led to an enhanced metastatic phenotype.
50 n of cancer stem cells, and acquisition of a metastatic phenotype.
51 n mutants of p110alpha produce a more severe metastatic phenotype.
52 secondary sites, reproducing the LgyLRV1(+) metastatic phenotype.
53 lls have an increased invasive but decreased metastatic phenotype.
54 than p53 mutant mice and a gain-of-function metastatic phenotype.
55 the tissue repair function to enhance their metastatic phenotype.
56 to Myc tumors associated with the increased metastatic phenotype.
57 eutic and radiation resistance, and even the metastatic phenotype.
58 evade apoptotic cell death and to acquire a metastatic phenotype.
59 Maspin transcription, thereby promoting the metastatic phenotype.
60 may provide a new approach to targeting the metastatic phenotype.
61 progression, with the goal of reversing the metastatic phenotype.
62 in rescued expression of KiSS-1 and reduced metastatic phenotype.
63 f which may undergo a reprogramming of their metastatic phenotype.
64 an important role in the development of the metastatic phenotype.
65 with a drug-resistant, highly invasive, and metastatic phenotype.
66 eregulate adhesion signaling and mediate the metastatic phenotype.
67 cell lines (M-4A4 and NM-2C5) with opposite metastatic phenotypes.
68 are often associated with more invasive and metastatic phenotypes.
69 ticularly in the development of invasive and metastatic phenotypes.
70 icated in the acquisition of tumorigenic and metastatic phenotypes.
71 een low canonical AR output and SRC-promoted metastatic phenotypes.
72 our study examines the genetic evolution of metastatic phenotypes.
73 nce that Slug enhances both tumor growth and metastatic phenotypes.
74 ependent activation of genes associated with metastatic phenotypes.
75 rogram and suppressed their self renewal and metastatic phenotypes.
76 ases (PTPases) associated with oncogenic and metastatic phenotypes.
77 hatases that are implicated in oncogenic and metastatic phenotypes.
78 their ability to cause motile, invasive and metastatic phenotypes.
79 nsufficient for, acquisition of a detectable metastatic phenotype; 2) demonstrated that metastatic su
80 astoma (NB) cells from a metastatic to a non-metastatic phenotype, a previously unknown function for
81 ne expression signature that correlated with metastatic phenotype and highlighted several GTPase sign
82 on of the human melanocyte towards the brain-metastatic phenotype and that NT enhance the activity of
83 These results suggest that the bone-specific metastatic phenotypes and gene expression signature iden
84 (NSCLC) expresses a particularly aggressive metastatic phenotype, and patients with this disease hav
85 network and the acquisition of the invasive-metastatic phenotype, and we show here that HGF/SF-Met s
86 n mitotically active cells that promoted pro-metastatic phenotypes, and in advanced PCa proved to be
87 Estrogen independence and progression to a metastatic phenotype are hallmarks of therapeutic resist
88 the DNA base and backbone structures of the metastatic phenotype are indistinguishable from those of
91 e derived from the mouse model abrogates the metastatic phenotype but does not affect tumor growth.
92 n breast cancer cells with a highly invasive/metastatic phenotype but not in poorly invasive/nonmetas
93 wn-regulation of Fas was associated with the metastatic phenotype, but alterations in Fas expression
94 protein 2 (AGR2) has been associated with a metastatic phenotype, but its mechanism of action and co
99 cancer cells to hypoxia, which promotes the metastatic phenotype by reducing intercellular adhesion
100 s ever to successfully transfer the complete metastatic phenotype by somatic cell fusion and support
102 rodent gene mediating tumor progression and metastatic phenotypes, can be used to drive imaging repo
103 ll-length MUC1 displayed a less invasive and metastatic phenotype compared with control-transfected c
104 ree derivative human lines with increasingly metastatic phenotypes, designated FL1, FL2, and FL3, wer
105 igh fat intake promotes the emergence of the metastatic phenotype; further research is required to es
107 protein, S100A4, have been shown to cause a metastatic phenotype in at least three independent model
111 nd colon and bladder carcinomas and with the metastatic phenotype in carcinomas of the lung, breast,
112 ibit Snail expression and, consequently, the metastatic phenotype in DU-145 prostate cancer cells.
113 nonical NFkappaB pathway promotes a dormant, metastatic phenotype in ER(+) breast cancer and implicat
116 roblast development and the acquisition of a metastatic phenotype in genetically engineered mice with
117 expression of PSAP was able to suppress the metastatic phenotype in highly metastatic 4T1 and MDA-MB
118 s corresponds to lymphangitic carcinomatosis metastatic phenotype in human cancer patients, an extrem
119 y correlated with an apoptotic-resistant and metastatic phenotype in human colon carcinoma cell lines
121 evels of S100A4 have been shown to produce a metastatic phenotype in independent models of breast can
122 mplete dominance of its undifferentiated and metastatic phenotype in multiple somatic cell hybridizat
124 ther the effect of LPA on acquisition of the metastatic phenotype in ovarian cancer cells is mediated
126 ntegrin was sufficient to revert this highly metastatic phenotype in the MNNG-HOS model without signi
128 benign cell tine is sufficient to produce a metastatic phenotype in this particular rat mammary mode
129 poptotic resistance is often associated with metastatic phenotype in tumor cells and is considered a
131 and silencing of these genes attenuated the metastatic phenotype in vitro and lung colonization in v
132 ctivity in vitro and adopted an invasive and metastatic phenotype in vivo, inferring significance of
134 r their abilities to mediate tumorigenic and metastatic phenotypes in athymic nude mice when expresse
135 y Sirtuin factor SIRT7 as a key regulator of metastatic phenotypes in both epithelial and mesenchymal
136 or GPCR signaling, strongly correlates with metastatic phenotypes in both prostate cancer cell lines
139 s for CADM1, SPHK1, and YAP/TAZ in mediating metastatic phenotypes in vitro and in vivo Notably, phar
140 ession contributes to several aspects of the metastatic phenotype including survival in the anchorage
141 ar activities capable of contributing to the metastatic phenotype, including growth, motility, invasi
142 re, CD44s may be a critical component of the metastatic phenotype induced by specific oncogenes.
143 MM activity was sufficient and necessary for metastatic phenotypes induced by RB loss in prostate can
144 rated that the transition of melanoma to the metastatic phenotype is associated with a loss of expres
145 hat the progression of human melanoma to the metastatic phenotype is associated with loss of AP-2 exp
148 ortant early event in the development of the metastatic phenotype is the induction of genes that prom
149 integral membrane mucin associated with the metastatic phenotype, is overexpressed by most human car
150 essed the growth of Lewis lung carcinoma-low metastatic phenotype metastases in C57BL/6 mice by great
152 demonstrate a strong correlation between the metastatic phenotype of a cell and its IL-8 expression,
153 highly relevant to human cancer and that the metastatic phenotype of a tumor may be affected by the g
158 of mechanisms that impede the aggressive and metastatic phenotype of human basal triple-negative-type
161 eptor, which subsequently contributes to the metastatic phenotype of melanoma by upregulating the exp
163 ession in PAR1-silenced cells fully restores metastatic phenotype of melanoma, indicating that PAFR p
164 may be relevant to the hormone-insensitive, metastatic phenotype of most advanced adenocarcinomas of
167 Kras(G12D) leading to an invasive and widely metastatic phenotype of pancreatic ductal adenocarcinoma
177 itro model which displayed the signatures of metastatic phenotype such as migration, invasiveness, ch
178 imus do not appear to have a more aggressive metastatic phenotype than those whose disease progresses
179 cells can exhibit a platelet-interactive and metastatic phenotype that is controlled by the activatio
180 on by tumor cells has been associated with a metastatic phenotype, the nature of the cellular target
181 tify the genes associated with the most lung-metastatic phenotype, the RNA complement from the parent
182 led miRNAs as suppressors of cell-autonomous metastatic phenotypes, the roles of non-coding RNAs in n
183 te bone marrow progenitor cells toward a pro-metastatic phenotype through MET" by Peinado and colleag
184 onsible for inducing specific aspects of the metastatic phenotype to allow for improved clinical dete
186 ion alone confers a transformed and in vitro metastatic phenotype to otherwise normal MCF-12A cells.
190 hanism of NPI-0052-induced inhibition of the metastatic phenotype was corroborated by: (1) treatment
191 in the progression of melanoma to the brain-metastatic phenotype, we determined whether NT stimulate
192 -function is critical for acquisition of the metastatic phenotype, we have compared the ability of Fa
194 that may be responsible for the invasive and metastatic phenotype, we used spectral karyotyping (SKY)
196 downregulation recapitulated miR-194-driven metastatic phenotypes, whereas overexpression of a nonta
197 rates with H-RAS to induce an aggressive and metastatic phenotype with the unusual occurrence of brai
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