戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 anoma has a poor prognosis due to its strong metastatic ability.
2 on, epithelial to mesenchymal transition and metastatic ability.
3 T24T cells significantly enhanced their lung metastatic ability.
4 ssed the effect of this treatment on in vivo metastatic ability.
5 istance of Mia(AR) and inhibited its in vivo metastatic ability.
6 as-resistant neoplastic clones with enhanced metastatic ability.
7 r resistance to anoikis could increase their metastatic ability.
8 should be associated with the acquisition of metastatic ability.
9 on, hyaluronate binding, tumorigenicity, and metastatic ability.
10 ival cues that helps explain their increased metastatic ability.
11 DSCs) showed enhanced cancer cell growth and metastatic ability.
12 hanges in LKB1-deficient cells that enhances metastatic ability.
13 ive and immunosuppressive traits and in vivo metastatic abilities.
14 xpressed in melanoma cells with high vs. low metastatic abilities.
15 is during the acquisition of tumorigenic and metastatic abilities.
16 , and the acquisition and diversification of metastatic abilities.
17 might modulate the effect of S100A4 on their metastatic abilities.
18 entiate prostate cancer cells with different metastatic abilities.
19 detecting prostate cancer cells of different metastatic abilities.
20 3 mutations endow tumor cells with increased metastatic ability, although our understanding of the un
21 re years are required for the acquisition of metastatic ability and patients die an average of two ye
22  human cancers has been correlated with high metastatic ability and poor prognosis.
23 rlying prostate cancer recurrence, increased metastatic ability and poorer prognosis after tumors hav
24 ntify a transcriptional program that confers metastatic ability and predicts patient survival.
25  stem cell-like properties, enhanced in vivo metastatic ability, and generated tumors rich in Gr1hiLy
26 on correlated with metabolic signaling, bone metastatic ability, and poor clinical outcomes.
27 es of two breast cancer cells with different metastatic ability at the site of bone metastases, using
28                           The acquisition of metastatic ability by tumor cells is considered a late e
29              Corresponding to their enhanced metastatic ability, CD24(+)CD29(+) cells exhibited featu
30  to the tumor matrix and tumors of differing metastatic ability differ in both tumor- and stroma-deri
31                                     Enhanced metastatic ability due to increased expression of ErbB2
32 of CaP cell lines revealed cells with a high metastatic ability exhibited increased Rap1 activity and
33 esultant transfectants were tested for their metastatic ability in athymic nude mice.
34 is, is predictive of aggressive behavior and metastatic ability in human breast cancers.
35 odifies the transformed phenotype and alters metastatic ability in immortal human melanocytes and met
36 cular changes associated with acquisition of metastatic ability in ovarian cancer are poorly understo
37 h, we identify CBFbeta as a key regulator of metastatic ability in the intermediate state.
38  significantly decreased their migratory and metastatic ability in vitro and in vivo.
39                       Arntl2 is required for metastatic ability in vivo and clonal growth in cell cul
40 pairs cell migration in culture and inhibits metastatic ability in vivo.
41 veral phenotypic changes including increased metastatic ability in vivo.
42 tion, we uncovered several key regulators of metastatic ability, including an actionable pro-metastat
43 se to varying types of signaling that affect metastatic ability, including the HRG-erbB pathway and t
44 these genes are inactivated in both alleles, metastatic ability is promoted.
45 molecular and cellular changes that regulate metastatic ability is required.
46                      Moreover, this enhanced metastatic ability is reversible and dependent on CCL5 s
47                                This enhanced metastatic ability is reversible and is dependent on CCL
48 r most cancer cell types, the acquisition of metastatic ability leads to clinically incurable disease
49 highly invasive cell phenotype and increased metastatic ability, mediated by interactions between Lam
50 , respectively, and significantly suppressed metastatic abilities of breast cancer cells.
51  to mitochondrial fragmentation and enhanced metastatic abilities of breast cancer cells.
52 rations in BMP signaling on the invasive and metastatic abilities of CRC cells and changes in members
53     USP13 also increased the tumorigenic and metastatic abilities of primary murine ovarian cancer ce
54 pression also directly increased the in vivo metastatic abilities of the LNCaP cells from the prostat
55 regation enhances the stemness, survival and metastatic ability of aggregated cells.
56 ome 16 has a strong activity to suppress the metastatic ability of AT6.1 cells while it did not affec
57 n chromosome 17 significantly suppresses the metastatic ability of AT6.1 rat prostate cancer cells wi
58 ce of this region suppresses the spontaneous metastatic ability of AT6.1 rat prostatic cancer cells b
59 l a role for histone H2AX in controlling the metastatic ability of breast cancer cells via maintenanc
60 tes and, as a direct consequence, govern the metastatic ability of carcinoma cells.
61 he stem-like cell population, migration, and metastatic ability of epithelial HCC cells.
62 ng, and overexpression of FOXC2 enhances the metastatic ability of mouse mammary carcinoma cells.
63 conclude that the BM-MSCs-mediated increased metastatic ability of PCa cells can be due to the PCa st
64             We also found that the increased metastatic ability of PCa cells could be due to the incr
65 s could recruit BM-MSCs and consequently the metastatic ability of PCa cells was increased.
66 opulation increase and thereby inhibited the metastatic ability of PCa cells.
67  CD133 and CXCR4 molecules, and enhanced the metastatic ability of PCa cells.
68    Inhibition of sialylation counteracts the metastatic ability of Phgdh(low) cancer cells.
69 ther, constitutively active CFL elevated the metastatic ability of prostate cancer cells in vivo.
70   The presence of this region suppresses the metastatic ability of rat prostate cancer cells.
71 onal gene expression programs and drives the metastatic ability of SCLC cells.
72 lular mechanism that contributes to the high metastatic ability of SCLC.
73 fic metastatic sites and results in enhanced metastatic ability of several tumors.
74                                          The metastatic ability of six representative clones was test
75                                 In parallel, metastatic ability of the alpha1,2FT-transfected BL6-2 c
76  of the standard CD44 isoform suppresses the metastatic ability of the AT3.1 Dunning subline without
77  binding; however, it equally suppressed the metastatic ability of the AT3.1 prostate cancer cells.
78                                  Whereas the metastatic ability of the AT6.1-MKK4/SEK1 cells was sign
79 ressed in many cancers and contribute to the metastatic ability of the cancer cells.
80 here it contributes to the proliferative and metastatic ability of the cancer cells.
81                                 However, the metastatic ability of the MoVi transfectants remained un
82                                          The metastatic ability of the resultant microcell hybrid clo
83     However, RhoC significantly enhanced the metastatic ability of the tumor cells in these animals,
84 ng only a weak correlation with the reported metastatic ability of these tumor cell lines.
85 (NO) synthase II (NOS II) expression and the metastatic ability of tumor cells is inconclusive.
86 DON decreased the self-renewal potential and metastatic ability of tumor cells.
87 f NOS II expression directly correlates with metastatic ability of UV-2237 fibrosarcoma cells carryin
88 de synthase II (NOS II) inducibility and the metastatic ability of UV-2237 murine fibrosarcoma cells
89 mation playing a major role in affecting the metastatic ability of uveal melanomas.
90  levels of SIMA135/CDCP1 correlated with the metastatic ability of variant HEp3 cell lines.
91     Increased levels of S100A4 (p9Ka) confer metastatic ability on a normally non-metastatic epitheli
92 arly dissemination process using preexisting metastatic ability rather than an evolution model.
93 y resistant to anoikis and manifested higher metastatic ability than S91Adh cells.
94 RhoGDI2 was transferred back into cells with metastatic ability that lacked its expression, it suppre
95 ant/refractory subline displayed significant metastatic ability, the parental line from which it was
96     Ectopic expression of miR-200 can confer metastatic ability to poorly metastatic tumor cells in s
97 in which one mutation is necessary to confer metastatic ability to the cell.
98 rat prostatic cells greatly suppresses their metastatic ability to the lungs without suppression of t
99 7 was silenced in breast cancer cells, their metastatic ability was inhibited.
100 Liver-metastasis variants having low to high metastatic ability were also established using in vivo/i
101  in human colon cancer cells of high and low metastatic ability were manipulated via expression of ga
102 ever, the phenotypes of NOS II induction and metastatic ability were unstable.
103        In breast cancers, the acquisition of metastatic ability, which is responsible for tumor relap
104 l is associated with the acquisition of high metastatic ability within the Dunning R-3327 system of r
105 f prostate cancer cells and suppressed their metastatic ability without suppressing their tumorigenic
106 e resulted in significant suppression of the metastatic ability without suppression of the tumorigeni

 
Page Top