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 s phosphoinositide 3-kinase, AKT, and SRC in highly metastatic cells.
2 n upon miR-200 overexpression toward that of highly metastatic cells.
3 elta levels were relatively increased in the highly metastatic cells.
4 r cassette exons with increased inclusion in highly metastatic cells.
5  transcripts displaying reduced stability in highly metastatic cells.
6 gainst poorly metastatic cells compared with highly metastatic cells.
7 ignificantly impairs the bone progression of highly metastatic cells.
8 g ligand activation of the EGFR, but only in highly-metastatic cells.
9 ecause they preferentially activate c-Src in highly-metastatic cells.
10              Within minutes of adhesion, the highly metastatic cells acquire the ability of enhanced
11 subset of drug-resisting, self-renewing, and highly metastatic cells called tumor initiating cells or
12 ere we show that loss of c-KIT expression in highly metastatic cells correlates with loss of expressi
13 at up-regulation of MCAM/MUC18 expression in highly metastatic cells correlates with loss of expressi
14 etastatic variants, suggest that not only do highly-metastatic cells display constitutively elevated
15 ration of miR-10b antagomirs to mice bearing highly metastatic cells does not reduce primary mammary
16                                              Highly metastatic cells evade this tumor-suppressive pat
17 ompared with poorly metastatic cancer cells, highly metastatic cells expressed increased levels of th
18                                              Highly metastatic cells growing in culture constitutivel
19                                              Highly metastatic cells growing in the prostate expresse
20 usly shown that enforced c-KIT expression in highly metastatic cells inhibited tumor growth and metas
21 ational regulator, and its downregulation in highly metastatic cells leads to the lengthening of 3' u
22                 Silencing of IL-13Ralpha2 in highly metastatic cells led to a decrease in adhesion ca
23 y a poorly metastatic cell line to that by a highly metastatic cell line 24 h after injection in the
24 -2 mRNA stabilization in MDA-MB-231 cells, a highly metastatic cell line derived from a human mammary
25 ential reversal of oncogenic properties of a highly metastatic cell line with the introduction of non
26 ially expressed (greater than 2-fold) in all highly metastatic cell lines relative to their reference
27                        The undifferentiated, highly metastatic cell lines with high metastatic potent
28                                              Highly metastatic cells (MDA-MB-435) expressing high lev
29            Does it arise from rare, variant, highly metastatic cells or does a primary tumor progress
30               We found that in vivo selected highly metastatic cell populations showed little genetic
31                      Introduction of Psap in highly metastatic cells significantly reduced the occurr
32                               Loss of CC3 in highly metastatic cells such as SCLC might render them r
33                                              Highly metastatic cells survived to produce numerous lun
34                                     When the highly metastatic cells were compared with their low met
35     We found that HNRNPC is downregulated in highly metastatic cells, which causes HNRNPC-bound mRNAs
36  kinase expression was first demonstrated in highly metastatic cells, whilst re-expression of the pro
37                    The pH at the surfaces of highly metastatic cells within tumors was found to be ab