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1 anoma has a poor prognosis due to its strong metastatic ability.
2 T24T cells significantly enhanced their lung metastatic ability.
3 ssed the effect of this treatment on in vivo metastatic ability.
4 istance of Mia(AR) and inhibited its in vivo metastatic ability.
5 as-resistant neoplastic clones with enhanced metastatic ability.
6 r resistance to anoikis could increase their metastatic ability.
7 should be associated with the acquisition of metastatic ability.
8 on, hyaluronate binding, tumorigenicity, and metastatic ability.
9 xpressed in melanoma cells with high vs. low metastatic abilities.
10 is during the acquisition of tumorigenic and metastatic abilities.
11 , and the acquisition and diversification of metastatic abilities.
12 might modulate the effect of S100A4 on their metastatic abilities.
13 3 mutations endow tumor cells with increased metastatic ability, although our understanding of the un
14 re years are required for the acquisition of metastatic ability and patients die an average of two ye
16 rlying prostate cancer recurrence, increased metastatic ability and poorer prognosis after tumors hav
20 to the tumor matrix and tumors of differing metastatic ability differ in both tumor- and stroma-deri
22 of CaP cell lines revealed cells with a high metastatic ability exhibited increased Rap1 activity and
25 odifies the transformed phenotype and alters metastatic ability in immortal human melanocytes and met
26 cular changes associated with acquisition of metastatic ability in ovarian cancer are poorly understo
29 tion, we uncovered several key regulators of metastatic ability, including an actionable pro-metastat
30 se to varying types of signaling that affect metastatic ability, including the HRG-erbB pathway and t
35 r most cancer cell types, the acquisition of metastatic ability leads to clinically incurable disease
36 highly invasive cell phenotype and increased metastatic ability, mediated by interactions between Lam
39 rations in BMP signaling on the invasive and metastatic abilities of CRC cells and changes in members
40 pression also directly increased the in vivo metastatic abilities of the LNCaP cells from the prostat
41 ome 16 has a strong activity to suppress the metastatic ability of AT6.1 cells while it did not affec
42 n chromosome 17 significantly suppresses the metastatic ability of AT6.1 rat prostate cancer cells wi
43 ce of this region suppresses the spontaneous metastatic ability of AT6.1 rat prostatic cancer cells b
45 ng, and overexpression of FOXC2 enhances the metastatic ability of mouse mammary carcinoma cells.
46 conclude that the BM-MSCs-mediated increased metastatic ability of PCa cells can be due to the PCa st
51 ther, constitutively active CFL elevated the metastatic ability of prostate cancer cells in vivo.
57 of the standard CD44 isoform suppresses the metastatic ability of the AT3.1 Dunning subline without
58 binding; however, it equally suppressed the metastatic ability of the AT3.1 prostate cancer cells.
67 f NOS II expression directly correlates with metastatic ability of UV-2237 fibrosarcoma cells carryin
68 de synthase II (NOS II) inducibility and the metastatic ability of UV-2237 murine fibrosarcoma cells
71 Increased levels of S100A4 (p9Ka) confer metastatic ability on a normally non-metastatic epitheli
73 RhoGDI2 was transferred back into cells with metastatic ability that lacked its expression, it suppre
74 ant/refractory subline displayed significant metastatic ability, the parental line from which it was
75 Ectopic expression of miR-200 can confer metastatic ability to poorly metastatic tumor cells in s
77 rat prostatic cells greatly suppresses their metastatic ability to the lungs without suppression of t
79 Liver-metastasis variants having low to high metastatic ability were also established using in vivo/i
80 in human colon cancer cells of high and low metastatic ability were manipulated via expression of ga
83 l is associated with the acquisition of high metastatic ability within the Dunning R-3327 system of r
84 f prostate cancer cells and suppressed their metastatic ability without suppressing their tumorigenic
85 e resulted in significant suppression of the metastatic ability without suppression of the tumorigeni
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