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 ith 15 to 25 mg lenalidomide and 15 to 20 mg CCI-779.
2 termined to be 25 mg lenalidomide with 15 mg CCI-779.
3 al protection in cells exposed to micromolar CCI-779.
4 thasone was combined with the mTOR inhibitor CCI-779.
5 s target in xenografted human ALL exposed to CCI-779.
6 mors regressed in response to treatment with CCI-779.
7  by the mTOR-specific blockers rapamycin and CCI-779.
8 activity and relatively mild side effects of CCI-779.
9 ycin (mTOR) inhibitors such as rapamycin and CCI-779.
10 graft model following in vivo treatment with CCI-779.
11 ich tumors will be sensitive or resistant to CCI-779.
12  FRAP/mTOR by using the rapamycin derivative CCI-779.
13    In this study, two doses of temsirolimus (CCI-779), a novel inhibitor of the mammalian target of r
14 hesis, we challenged myeloma cell lines with CCI-779, a newly developed analogue of rapamycin and an
15  on bone marrow stroma and were treated with CCI-779, a second generation MTI.
16  treated Pten conditional knockout mice with CCI-779, a specific mTor inhibitor.
17 generated from the same patient samples with CCI-779 after establishment of disease.
18 addition, exposure of abl and C4-2B cells to CCI-779 also decreased UBE2C-dependent cell invasion.
19                               Interestingly, CCI-779 also produced growth inhibition of xenografts de
20 ed whether temsirolimus (previously known as CCI-779), an inhibitor of the mammalian target of rapamy
21 ed that the G(1)-S cell-cycle inhibitor-779 (CCI-779), an mTOR inhibitor, inhibited UBE2C mRNA and pr
22                           Both rapamycin and CCI-779, an ester analog of rapamycin with improved phar
23 egative PC-3 prostate cancer xenografts with CCI-779, an ester of rapamycin in clinical development c
24                                              CCI-779, an mTOR inhibitor, arrested growth of a phospha
25 es greater after simultaneous treatment with CCI-779 and cisplatin than after cisplatin alone.
26                   Combination treatment with CCI-779 and HCQ suppressed melanoma growth and induced c
27 tor hydroxychloroquine (HCQ) synergizes with CCI-779 and led to melanoma cell death via apoptosis.
28 ectly related to the antitumor activities of CCI-779 and other rapalogues in human cancer patients.
29               Rapamycin and its derivatives, CCI-779 and RAD001 (designated rapamycins), specifically
30       Rapamycin and several analogs, such as CCI-779 and RAD001, are currently undergoing clinical ev
31            Biochemical assays indicated that CCI-779 and rapamycin directly inhibited mTOR kinase act
32 he rapamycin derivatives (RDs) temsirolimus (CCI-779) and everolimus (RAD001) in acute myeloid leukem
33 o specific allosteric inhibitors (rapamycin, CCI-779, and RAD001) of the pivotal cell growth regulato
34 r cell types, and its derivatives RAD001 and CCI-779 are currently in phase I and phase II clinical t
35                                   RAD001 and CCI-779 are in phase I and II trials, respectively, as a
36  trial using targeted molecular therapy with CCI-779 as a single agent for mTOR-activated residual ce
37                     In cell culture studies, CCI-779 at the commonly used nanomolar concentrations ge
38 DA-approved rapamycin analogue temsirolimus (CCI-779) blocks ANDV protein expression and virion relea
39                          Thus, rapamycin and CCI-779, by interacting with downstream intermediates in
40 cin) pathway using rapamycin or its analogue CCI-779 can improve the cellular and behavioural phenoty
41 cromolar but not nanomolar concentrations of CCI-779 caused a marked decline in global protein synthe
42         In those animals that formed tumors, CCI-779 caused a significant decrease in the tumor volum
43 ective pharmacologic inhibitor, Ku0063794 or CCI-779, caused the up-regulation of nuclear phospho-Mst
44 block cell-cycle G(1) to S-phase transition, CCI-779 causes a cell-cycle G(2)-M accumulation and an i
45 ally relevant low micromolar concentrations, CCI-779 completely suppressed proliferation of a broad p
46                      Growth arrest caused by CCI-779 correlates with a block in translation of mRNA e
47 malian target of rapamycin (mTOR) inhibitor, CCI-779, curtailed the growth of a subcutaneous challeng
48                                     In vivo, CCI-779 delayed DAOY xenograft growth by 160% after 1 we
49 nor efficacy was significantly influenced by CCI-779 dose level.
50                                              CCI-779, given as 10 intraperitoneal injections, induced
51                                              CCI-779 has completed several phase I clinical evaluatio
52 tion of lenalidomide with the mTOR inhibitor CCI-779 has displayed synergy in vitro and represents a
53 Huntington disease, and the rapamycin analog CCI-779 improved performance on four different behaviora
54 ignificance of this pathway was tested using CCI-779 in a mouse xenograft model.
55 this potential, we used the rapamycin analog CCI-779 in a myeloma xenograft model.
56               We also assessed the effect of CCI-779 in a NOD/SCID xenograft model.
57 suppressant agent rapamycin and its analogue CCI-779 in human brain tumor cell lines in vitro and in
58  into possible therapeutic uses of rapamycin/CCI-779 in the treatment of neurodegenerative diseases (
59 which contributes to antitumor activities of CCI-779 in UBE2C overexpressed AR-positive CRPC.
60 ayed an 11-fold resistance to the micromolar CCI-779 in vitro (IC(50), 20 +/- 3.4 micromol/L) and con
61 es kidney cancer cells to the mTOR inhibitor CCI-779 in vitro and in mouse models.
62 s(LA1) mice, was resistant to treatment with CCI-779 in vitro.
63  particular the mTOR inhibitor temsirolimus (CCI-779), induce autophagy, which can promote tumor surv
64  activation were particularly sensitive to a CCI-779-induced antitumor response.
65                                     However, CCI-779 inhibited expression of c-myc in CCI-sensitive P
66                                              CCI-779 inhibited growth of established tumors in nude m
67                 The molecular mechanisms for CCI-779 inhibition of UBE2C gene expression involved a d
68        These findings suggest that high-dose CCI-779 inhibits mTOR signaling through an FKBP12-indepe
69  studies suggest that the rapamycin analogue CCI-779 is an important new agent to investigate in the
70 biomechanical fluidic environment of the BM, CCI-779 is equally effective in inhibiting BM endothelia
71                                Temsirolimus (CCI-779) is a small-molecule inhibitor of the mammalian
72 r cells with WYE-132 or the rapamycin analog CCI-779 led to a rapid loss of the phosphorylation at Se
73                                     Although CCI-779-mediated inhibition of the p70 mTOR substrate wa
74 own promise in early clinical trials such as CCI-779, pegylated interferon, thalidomide, and anti-VEG
75          Similar and significant changes for CCI-779 pharmacokinetics were also observed with increas
76    Blood samples were collected to determine CCI-779 pharmacokinetics.
77                                              CCI-779 produced an objective response rate of 7% (one c
78 ice by treatment with the rapamycin analogue CCI-779 reduced the size and number of early epithelial
79                The most frequently occurring CCI-779-related adverse events of all grades were maculo
80                             Interestingly, a CCI-779-resistant mTOR mutant (mTOR-SI) displayed an 11-
81 ssion of a constitutively active AKT gene in CCI-779-resistant myeloma cells containing wild-type PTE
82 target of rapamycin inhibitors rapamycin and CCI-779 resulted in inhibition of IL-6-induced myeloma c
83 inetic analysis indicated increased doses of CCI-779 resulted in statistically significant changes in
84 inical interactions between lenalidomide and CCI-779 seemed to occur, with in vitro data indicating l
85 nd quiescent AKT did not convert them to the CCI-779-sensitive phenotype.
86  Conversely, expression of wild-type PTEN in CCI-779-sensitive, PTEN-deficient myeloma cells did not
87 se down-regulation is required for rapamycin/CCI-779 sensitivity.
88                         Animals treated with CCI-779 showed a decrease in peripheral-blood blasts and
89               In patients with advanced RCC, CCI-779 showed antitumor activity and encouraging surviv
90                               Treatment with CCI-779 significantly decreased abl cell proliferation i
91           The Kaplan-Meier curve showed that CCI-779 significantly increased survival (P < 0.0001).
92                                              CCI-779 suppressed phosphorylation of mTOR downstream pr
93 mmalian target of rapamycin (mTOR) inhibitor CCI-779 (temsirolimus) is a recently Food and Drug Admin
94 atter cells was remarkably more sensitive to CCI-779 than the growth of control U266 cells.
95            The mTOR inhibitors rapamycin and CCI-779, the PI3-kinase inhibitor LY294002, and the MEK
96 r to be due to differences in the ability of CCI-779 to inhibit mTOR and induce dephosphorylation of
97  Akt in PTEN(+/+) cells also was reversed by CCI-779 treatment, indicating that FRAP/mTOR functions d
98                  Differential sensitivity to CCI-779 was not explained by differences in biochemical
99 ndomly assigned to receive 25, 75, or 250 mg CCI-779 weekly as a 30-minute intravenous infusion.
100                           Effective doses of CCI-779 were associated with modest toxicity, inducing o
101 iferase allowed us to monitor the effects of CCI-779 with bioluminescence imaging in the MRD model.
102  to cytoreduction and G(1) arrest induced by CCI-779 with ID(50) concentrations of <1 nM.
103 on regimen was 25 mg lenalidomide with 15 mg CCI-779, with toxicities of fatigue, neutropenia, and el
104       Compared with the rapalog temsirolimus/CCI-779, WYE-132 elicited a substantially stronger inhib

 
Page Top