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1 d nonmutagenic and consequently described as nongenotoxic.
2                     Results suggest that the nongenotoxic activation of p53 by targeting the Mdm2-p53
3 eraction between p53 and Mdm2 results in the nongenotoxic activation of p53, the authors sought to in
4 therapeutics, including PARP inhibitors, and nongenotoxic activation of p53.
5 oposide or 300 mM N-methylformamide (NMF), a nongenotoxic agent.
6 oliferators, a group of structurally diverse nongenotoxic agents, induce predictable pleiotropic resp
7                                            A nongenotoxic AhR ligand (2,3,7,8-tetrachlorodibenzo-p-di
8 inally, a structurally related cytotoxic but nongenotoxic analog of DCVC did not induce c-myc and did
9 ers are aneuploid, that many carcinogens are nongenotoxic, and that mutated genes from cancer cells d
10 tore the functional p53 constitute potential nongenotoxic anticancer agents with a novel mode of acti
11 ecule antagonists could provide an efficient nongenotoxic anticancer therapy.
12       Phenobarbital (PB) is the prototype of nongenotoxic cacinogens that promote HCC in rodents.
13 in vitro models for developing genotoxic and nongenotoxic cancer therapies for reactivating p53 trans
14           Phorbol 12-myristate 13-acetate, a nongenotoxic carcinogen that is not classified as a pero
15        For decades, arsenic was considered a nongenotoxic carcinogen.
16                 Peroxisome proliferators are nongenotoxic carcinogens capable of causing rapid transc
17 eroxisome proliferators (PPs) are a class of nongenotoxic carcinogens in the rodent liver.
18 e mode of action by which phenobarbital-like nongenotoxic carcinogens promote liver tumor formation i
19   In addition to PB, many CAR activators are nongenotoxic carcinogens, but the role of CAR in liver t
20 arkers to facilitate early identification of nongenotoxic carcinogens.
21 roliferation characteristic of this class of nongenotoxic carcinogens.
22 ize mutation of cellular genes, we have used nongenotoxic carcinogens.
23 D117/LNP affected HSC function and permitted nongenotoxic conditioning for HSCT.
24  The ability to target HSCs in vivo offers a nongenotoxic conditioning regimen for HSCT, and this pla
25  improve multilineage engraftment; we tested nongenotoxic conditioning with anti-CD45 mAbs conjugated
26                                 TNF-alpha, a nongenotoxic cytokine, also induced the expression of KI
27 e to different doses of a well-characterized nongenotoxic hepatocarcinogen, phenobarbital, in rats.
28 e it is absent in HeLa cells challenged with nongenotoxic hydrocarbon carcinogens.
29 -/- cells to interferon-gamma (IFN-gamma), a nongenotoxic immune-regulatory cytokine, enhances engraf
30 onversion in cells treated with nutlin-3a, a nongenotoxic inducer of p53, in cell lines susceptible t
31 is robustly induced by various genotoxic and nongenotoxic insults in a p53-dependent manner.
32 odels, owing to its ability to bind DNA in a nongenotoxic manner and inactivate the FACT chromatin mo
33       Our findings favor an involvement of a nongenotoxic mechanism in tamoxifen-associated human end
34 t was optimized into a potent, specific, and nongenotoxic molecule called UM4118.
35 pothesized that IFN-gamma may be useful as a nongenotoxic, myelopreparative conditioning agent.
36                   The series was found to be nongenotoxic, nonmutagenic, devoid of mitochondrial toxi
37                                         Both nongenotoxic (nutlin-3a) and genotoxic (melphalan) p53-i
38 nvestigated the potential therapeutic use of nongenotoxic p53 activation by a small-molecule antagoni
39 ts of combined MEK inhibition by AZD6244 and nongenotoxic p53 activation by MDM2 antagonist Nutlin-3a
40 on does not affect the apoptotic response to nongenotoxic p53 activation.
41 e selective MDM2 antagonist, nutlin-3a, as a nongenotoxic p53 activator and show that the cell-cycle
42 carcinogens promote cancer via genotoxic and nongenotoxic pathways, but nongenetic mechanisms remain
43 e proliferators (PPs) are a diverse group of nongenotoxic rodent liver carcinogens.
44                 Peroxisome proliferators are nongenotoxic rodent-liver carcinogens that have been sho
45 eutic agents which do not target topo II, or nongenotoxic stimuli of apoptotic cell death, suggesting
46  that IFN-gamma conditioning may be a useful nongenotoxic strategy for myelopreparation in FA patient
47 at IFN-gamma conditioning may be useful as a nongenotoxic strategy for myelopreparation in this disor
48  tumor cells to a wide range of genotoxic or nongenotoxic stress conditions.
49 ersistent genetic instability was induced by nongenotoxic stress exposures such as heat treatment, se
50                      Hypoxia is an important nongenotoxic stress that modulates the tumor suppressor
51                               In response to nongenotoxic stress, JNK phosphorylates Jun, an AP-1 tra
52 and -independent manner during genotoxic and nongenotoxic stress-induced apoptosis.
53 his study, we investigated how genotoxic and nongenotoxic stresses regulate p53 association with chro
54                  We found that genotoxic and nongenotoxic stresses result in the accumulation and bin
55 y CBP/p300 in response to genotoxic and some nongenotoxic stresses.
56        Peroxisome proliferators (PPs) act as nongenotoxic tumor promoters in rodents.