ライフサイエンスコーパス: nongenotoxic

1 Results suggest that the nongenotoxic activation of p53 by targeting the Mdm2-p53

2 eraction between p53 and Mdm2 results in the nongenotoxic activation of p53, the authors sought to in

3 therapeutics, including PARP inhibitors, and nongenotoxic activation of p53.

4 oposide or 300 mM N-methylformamide (NMF), a nongenotoxic agent.

5 oliferators, a group of structurally diverse nongenotoxic agents, induce predictable pleiotropic resp

6 A nongenotoxic AhR ligand (2,3,7,8-tetrachlorodibenzo-p-di

7 inally, a structurally related cytotoxic but nongenotoxic analog of DCVC did not induce c-myc and did

8 ers are aneuploid, that many carcinogens are nongenotoxic, and that mutated genes from cancer cells d

9 tore the functional p53 constitute potential nongenotoxic anticancer agents with a novel mode of acti

10 ecule antagonists could provide an efficient nongenotoxic anticancer therapy.

11 Phenobarbital (PB) is the prototype of nongenotoxic cacinogens that promote HCC in rodents.

12 in vitro models for developing genotoxic and nongenotoxic cancer therapies for reactivating p53 trans

13 Phorbol 12-myristate 13-acetate, a nongenotoxic carcinogen that is not classified as a pero

14 For decades, arsenic was considered a nongenotoxic carcinogen.

15 Peroxisome proliferators are nongenotoxic carcinogens capable of causing rapid transc

16 eroxisome proliferators (PPs) are a class of nongenotoxic carcinogens in the rodent liver.

17 In addition to PB, many CAR activators are nongenotoxic carcinogens, but the role of CAR in liver t

18 arkers to facilitate early identification of nongenotoxic carcinogens.

19 roliferation characteristic of this class of nongenotoxic carcinogens.

20 ize mutation of cellular genes, we have used nongenotoxic carcinogens.

21 TNF-alpha, a nongenotoxic cytokine, also induced the expression of KI

22 e to different doses of a well-characterized nongenotoxic hepatocarcinogen, phenobarbital, in rats.

23 e it is absent in HeLa cells challenged with nongenotoxic hydrocarbon carcinogens.

24 -/- cells to interferon-gamma (IFN-gamma), a nongenotoxic immune-regulatory cytokine, enhances engraf

25 onversion in cells treated with nutlin-3a, a nongenotoxic inducer of p53, in cell lines susceptible t

26 is robustly induced by various genotoxic and nongenotoxic insults in a p53-dependent manner.

27 odels, owing to its ability to bind DNA in a nongenotoxic manner and inactivate the FACT chromatin mo

28 Our findings favor an involvement of a nongenotoxic mechanism in tamoxifen-associated human end

29 pothesized that IFN-gamma may be useful as a nongenotoxic, myelopreparative conditioning agent.

30 Both nongenotoxic (nutlin-3a) and genotoxic (melphalan) p53-i

31 nvestigated the potential therapeutic use of nongenotoxic p53 activation by a small-molecule antagoni

32 ts of combined MEK inhibition by AZD6244 and nongenotoxic p53 activation by MDM2 antagonist Nutlin-3a

33 on does not affect the apoptotic response to nongenotoxic p53 activation.

34 e selective MDM2 antagonist, nutlin-3a, as a nongenotoxic p53 activator and show that the cell-cycle

35 e proliferators (PPs) are a diverse group of nongenotoxic rodent liver carcinogens.

36 Peroxisome proliferators are nongenotoxic rodent-liver carcinogens that have been sho

37 eutic agents which do not target topo II, or nongenotoxic stimuli of apoptotic cell death, suggesting

38 that IFN-gamma conditioning may be a useful nongenotoxic strategy for myelopreparation in FA patient

39 at IFN-gamma conditioning may be useful as a nongenotoxic strategy for myelopreparation in this disor

40 tumor cells to a wide range of genotoxic or nongenotoxic stress conditions.

41 ersistent genetic instability was induced by nongenotoxic stress exposures such as heat treatment, se

42 Hypoxia is an important nongenotoxic stress that modulates the tumor suppressor

43 In response to nongenotoxic stress, JNK phosphorylates Jun, an AP-1 tra

44 and -independent manner during genotoxic and nongenotoxic stress-induced apoptosis.

45 his study, we investigated how genotoxic and nongenotoxic stresses regulate p53 association with chro

46 We found that genotoxic and nongenotoxic stresses result in the accumulation and bin

47 y CBP/p300 in response to genotoxic and some nongenotoxic stresses.

48 Peroxisome proliferators (PPs) act as nongenotoxic tumor promoters in rodents.