ライフサイエンスコーパス: cytostasis

1 ffective therapy, which induced Rb-dependent cytostasis.

2 plete inhibition of Mphi-mediated tumor cell cytostasis.

3 t growth, and resistance to TGF-beta-induced cytostasis.

4 -induced inhibition of protein synthesis and cytostasis.

5 mor cells to heat-stable enterotoxin-induced cytostasis.

6 and is directly involved in the induction of cytostasis.

7 cyclic nucleotide accumulation required for cytostasis.

8 IGF-I-induced Akt phosphorylation to induce cytostasis.

9 Ser-490 are implicated in the regulation of cytostasis.

10 ing a role for gamma-PAK in the induction of cytostasis.

11 overexpression in those cells and increased cytostasis.

12 8 h of chemotherapy, before the induction of cytostasis.

13 hile the majority of cells undergo a form of cytostasis.

14 rnative mechanisms for antiestrogen-mediated cytostasis.

15 ration by NO donors was not due to metabolic cytostasis.

16 t a rise in cAMP is not sufficient to induce cytostasis.

17 PD 153035 caused dose-dependent cytostasis (200 nmol/L to 1 micromol/L) and apoptosis (>

18 3 phenotype was expressed and in Thy4 during cytostasis, a mp53 phenotype was manifested, as determin

19 d play an important role in cytotoxicity and cytostasis against many pathogenic microorganisms.

20 What determines the choice between cytostasis and apoptosis is not clear.

21 that SphK2 may influence the balance between cytostasis and apoptosis of human cancer cells.

22 of protein kinase activity but do not induce cytostasis and are not bound to the ER.

23 DETA-NONOate played an important role in the cytostasis and arrest of these tumor cells in the G(1) p

24 to rapamycin by decreasing rapamycin-induced cytostasis and autophagy.

25 tyrosine kinase inhibitor PD 153035 induces cytostasis and caspase-dependent apoptosis in EGFR ligan

26 impaired (1 micromol/L, 4-24 h), leading to cytostasis and cell cycle arrest within 24 h by decrease

27 n tomography ([18F]FLT-PET) to measure early cytostasis and cytotoxicity induced by cisplatin treatme

28 in parallel with phenotypic data on cellular cytostasis and cytotoxicity.

29 enotypes controlled by these states, such as cytostasis and death.

30 This NO-induced cytostasis and decrease in cyclin D1 was reversible for

31 nduce proliferation while high levels induce cytostasis and inhibition of protein synthesis.

32 itivity to phorbol myristate acetate-induced cytostasis and megakaryocytic differentiation, suggestin

33 therapy using miRNAs as agents that mediate cytostasis and promote muscle differentiation.

34 metry-based assay that is not biased against cytostasis and reduced cell number.

35 at CDK4/6 inhibition is a potent mediator of cytostasis and that RB loss can be readily compensated f

36 of action, including induction of apoptosis, cytostasis, and antiangiogenesis.

37 d EMT and invasion, restore TGFbeta-mediated cytostasis, and inhibit three-dimensional organoid growt

38 itor of HSP90, acting via several processes (cytostasis, apoptosis, invasion, and angiogenesis) to in

39 CCT018159 caused cell cytostasis associated with a G(1) arrest and induced apo

40 l line is simply an index of cytotoxicity or cytostasis, but the patterns of 60 such GI50 values enco

41 A-357300 induces cytostasis by cell cycle arrest at the G(1) phase select

42 A model for the induction of cytostasis by gamma-PAK through targeting of gamma-PAK t

43 stable enterotoxins induce colon cancer cell cytostasis by targeting guanylyl cyclase C (GCC) signali

44 Antiestrogens induce both cytostasis (cell cycle arrest) and apoptosis, but the re

45 ions seen in confluent replicon cells, i.e., cytostasis combined with a sharp decrease in replicon co

46 Neither cytotoxicity nor cytostasis correlated with expression of p21Waf1/Cip1 Th

47 work confers resistance to TGF-beta-mediated cytostasis during the development of the telencephalic n

48 cells, moreover, bypassed TGF-beta1-mediated cytostasis evident in control short hairpin RNA-expressi

49 ction with representative compounds inducing cytostasis in an SJSA-1 osteosarcoma xenograft model fol

50 Our results suggest that NO-induced cytostasis in breast cancer cells was due to PKR activat

51 WAF1 (p21) is important for TGFbeta-mediated cytostasis in epithelial cells but not in hematopoietic

52 lonogenic survival and induced apoptosis and cytostasis in formed tumor colonies.

53 is not mediated by apoptosis but results in cytostasis in four cell lines tested.

54 d variable apoptosis (>10 micromol/L) but no cytostasis in ligand-independent cell lines.

55 -NONOate, a nitric oxide (NO) donor, induced cytostasis in the human breast cancer cells MDA-MB-231,

56 P1 also inhibits gene expression and induces cytostasis in transfected cells when it is expressed at

57 adapt quickly to CDK4/6 inhibition and evade cytostasis, in part, via noncanonical cyclin D1-CDK2-med

58 laxis and bradyphylaxis restores cancer cell cytostasis induced by heat-stable enterotoxins.

59 HK1(-)HK2(+) cancer subsets are sensitive to cytostasis induced by HK2(shRNA) knockdown and are also

60 iated apoptotic block undergo a drug-induced cytostasis involving the accumulation of p53, p16(INK4a)

61 n receptor (ER+) breast cancer, and although cytostasis is frequently observed, new treatment strateg

62 iated by natural killer cells in vitro or to cytostasis mediated by macrophages than control transduc

63 as evident during TGFbeta-induced epithelial cytostasis, mesenchymal differentiation, and myofibrobla

64 TGF-beta-dependent cytostasis occurred in normal and cancer cells through p

65 because many new agents are thought to cause cytostasis rather than cytotoxicity.

66 ury and converted the reversible, NO-induced cytostasis response of cells to an apoptotic response.

67 TGF-beta1-induced renal epithelial cytostasis was also completely bypassed by Rac1, p22(pho

68 agents, early clinical data demonstrate only cytostasis when used as monotherapy.