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1 erexpression of CDK9 increased resistance to dinaciclib.
2  mimetics boosts the therapeutic efficacy of dinaciclib.
3 et frequently overexpressed in HCC, and with Dinaciclib, a clinically tested Cdk5 inhibitor is readil
4               Specifically, encapsulation of dinaciclib, a cyclin-dependent kinase inhibitor, into PD
5                  In this study, we show that dinaciclib, a potent cyclin dependent kinase inhibitor,
6                           As doxorubicin and dinaciclib also reduced BCL-XL, the combinations of BCL-
7                                              Dinaciclib also significantly sensitized NB cell lines t
8  inhibition, HB cell lines were treated with dinaciclib and evaluated with cytotoxic, cell-death reve
9              We found that the CDK inhibitor dinaciclib and HDAC inhibitor panobinostat were the most
10 that the synthetic lethal strategy employing dinaciclib and niraparib was also highly efficacious in
11                   Specific CDK inhibition by dinaciclib and palbociclib decreases PASMC proliferation
12                         Our results identify dinaciclib as a novel and potent therapeutic agent alone
13           Herein, we identified the pan-CDKi dinaciclib as a promising alternative to palbociclib for
14 ght the potential of multi-CDK inhibition by dinaciclib as an alternative option to CDK4/6 specific i
15 dependent kinase 9 inhibitors, alvocidib and dinaciclib as potent HB growth inhibitors for the high-r
16                                We found that dinaciclib had a marked effect on HB cell viability, ind
17 palbociclib and multi-CDK inhibitors such as dinaciclib have rejuvenated the field.
18  study demonstrates single agent activity of dinaciclib in relapsed myeloma, with 2 patients achievin
19                                 Importantly, dinaciclib, in combination with gemcitabine, produced a
20                                              Dinaciclib induced cytotoxicity through a mitochondrial-
21 expression of Mcl-1 protected AML cells from dinaciclib-induced apoptosis.
22                                              Dinaciclib is a novel potent small molecule inhibitor of
23 ing data and pathway analysis suggested that dinaciclib is a potent cell death inducer in MB cells.
24 K2 and CDK9 activity by small molecules like dinaciclib is a promising strategy and a treatment optio
25                                              Dinaciclib is a small molecule multi-CDK inhibitor targe
26 mpetitive inhibitors such as palbociclib and dinaciclib is presented, followed by a compilation of ne
27 ith a clinically relevant experimental drug, dinaciclib, led to potent RALB-dependent antileukemic ef
28 with placebo, vincristine + irinotecan (VI), dinaciclib, or VI + dinaciclib to evaluate tumor growth
29                                 Furthermore, dinaciclib potently suppressed the clonogenic potential
30 , or the administration of the CDK inhibitor dinaciclib, protected mice against polymicrobial sepsis
31 tor ABT-199 (venetoclax) with doxorubicin or dinaciclib provided effective therapeutic strategies for
32 h either TEPP-46 or the potent CDK inhibitor dinaciclib reduced tumor growth and diminished PKM2pS37.
33                                     Notably, dinaciclib resensitized TBNC cells, which had acquired r
34        In our PDX model, treatment with VI + dinaciclib resulted in decreased tumor volume, viability
35 atment of MLL-rearranged leukemic cells with dinaciclib resulted in rapidly decreased expression of t
36                                 Furthermore, dinaciclib revealed in vivo antitumor efficacy in an ort
37               We present evidence supporting dinaciclib's ability to inhibit MB cells in vitro prolif
38 we show that a novel multiple-CDK inhibitor, dinaciclib (SCH727965, MK-7965), exhibits potent anti-pr
39  findings, combination treatment with VI and dinaciclib should be investigated further as a treatment
40                               Treatment with dinaciclib significantly suppressed cell proliferation,
41                                              Dinaciclib suppressed expression of its molecular target
42 ng doxorubicin and CDK9 inhibitors including dinaciclib that synergized with ABT-263 through downregu
43 stine + irinotecan (VI), dinaciclib, or VI + dinaciclib to evaluate tumor growth and response to ther
44  evaluating the combination of sorafenib and Dinaciclib to improve the therapeutic situation for pati
45                            Administration of dinaciclib to mice bearing MLL-AF9-driven human and mous
46 nations including Afuresertib + Palbociclib, Dinaciclib + Trametinib, Afatinib + Oxaliplatin, Ulixert
47                                We found that dinaciclib-triggered apoptosis is triggered by CDK9 inhi
48                                              Dinaciclib was administered on day 1 of a 21-day cycle a
49   In this study, the therapeutic efficacy of dinaciclib was assessed using patient-derived xenograft
50 atment with GSK2334470 or the CDK2 inhibitor dinaciclib was sufficient to reverse these events and to
51  Using the cyclin-dependent kinase inhibitor dinaciclib, which downregulates MYC expression, we found
52 ic mediator for MB cells and co-treatment of dinaciclib with BH3 mimetics boosts the therapeutic effi
53                              Combinations of dinaciclib with TEPP-46 reduced cell invasion, impaired
54 g Brd4 and CDK concurrently with AZD5153 and dinaciclib would be most effective in tumor growth suppr