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1 plete inhibition of Mphi-mediated tumor cell cytostasis.
2 t growth, and resistance to TGF-beta-induced cytostasis.
3 -induced inhibition of protein synthesis and cytostasis.
4 mor cells to heat-stable enterotoxin-induced cytostasis.
5 and is directly involved in the induction of cytostasis.
6 cyclic nucleotide accumulation required for cytostasis.
7 IGF-I-induced Akt phosphorylation to induce cytostasis.
8 Ser-490 are implicated in the regulation of cytostasis.
9 ing a role for gamma-PAK in the induction of cytostasis.
10 overexpression in those cells and increased cytostasis.
11 8 h of chemotherapy, before the induction of cytostasis.
12 hile the majority of cells undergo a form of cytostasis.
13 rnative mechanisms for antiestrogen-mediated cytostasis.
14 ration by NO donors was not due to metabolic cytostasis.
15 ffective therapy, which induced Rb-dependent cytostasis.
17 3 phenotype was expressed and in Thy4 during cytostasis, a mp53 phenotype was manifested, as determin
22 DETA-NONOate played an important role in the cytostasis and arrest of these tumor cells in the G(1) p
24 tyrosine kinase inhibitor PD 153035 induces cytostasis and caspase-dependent apoptosis in EGFR ligan
25 impaired (1 micromol/L, 4-24 h), leading to cytostasis and cell cycle arrest within 24 h by decrease
26 n tomography ([18F]FLT-PET) to measure early cytostasis and cytotoxicity induced by cisplatin treatme
31 itivity to phorbol myristate acetate-induced cytostasis and megakaryocytic differentiation, suggestin
34 at CDK4/6 inhibition is a potent mediator of cytostasis and that RB loss can be readily compensated f
36 d EMT and invasion, restore TGFbeta-mediated cytostasis, and inhibit three-dimensional organoid growt
37 itor of HSP90, acting via several processes (cytostasis, apoptosis, invasion, and angiogenesis) to in
39 l line is simply an index of cytotoxicity or cytostasis, but the patterns of 60 such GI50 values enco
42 stable enterotoxins induce colon cancer cell cytostasis by targeting guanylyl cyclase C (GCC) signali
44 ions seen in confluent replicon cells, i.e., cytostasis combined with a sharp decrease in replicon co
46 work confers resistance to TGF-beta-mediated cytostasis during the development of the telencephalic n
47 cells, moreover, bypassed TGF-beta1-mediated cytostasis evident in control short hairpin RNA-expressi
49 WAF1 (p21) is important for TGFbeta-mediated cytostasis in epithelial cells but not in hematopoietic
53 -NONOate, a nitric oxide (NO) donor, induced cytostasis in the human breast cancer cells MDA-MB-231,
54 P1 also inhibits gene expression and induces cytostasis in transfected cells when it is expressed at
55 adapt quickly to CDK4/6 inhibition and evade cytostasis, in part, via noncanonical cyclin D1-CDK2-med
57 iated apoptotic block undergo a drug-induced cytostasis involving the accumulation of p53, p16(INK4a)
58 iated by natural killer cells in vitro or to cytostasis mediated by macrophages than control transduc
61 ury and converted the reversible, NO-induced cytostasis response of cells to an apoptotic response.
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