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1  attributed to a cell-autonomous process of 'oncogene-induced senescence'.
2 upporting cancer cell growth and suppressing oncogene-induced senescence.
3 gnalling during the stress-response phase of oncogene-induced senescence.
4 RAS-induced DNA damage and thereby reinforce oncogene-induced senescence.
5 ation, but too strong a signal may result in oncogene-induced senescence.
6 and those that are excluded, likely encoding oncogene-induced senescence.
7  a causative factor underlying "escape" from oncogene-induced senescence.
8 or type 1 (AT(1)-R) in normal cells inhibits oncogene-induced senescence.
9 e an irreversible cell cycle arrest known as oncogene-induced senescence.
10 an tumors, and show coincident regulation in oncogene-induced senescence.
11 nd p38alpha contribute to MSK1 activation in oncogene-induced senescence.
12 n addition NR2E1 expression also counteracts oncogene-induced senescence.
13 ted by oncogenic stress, and is required for oncogene-induced senescence.
14 H1 loss provokes DNA damage and induction of oncogene-induced senescence.
15 t remains unclear whether they can influence oncogene-induced senescence.
16 ally due to NF-kappaB-mediated abrogation of oncogene-induced senescence.
17 ivates UCA1, revealing a novel mechanism for oncogene-induced senescence.
18 th an elevation in both apoptosis as well as oncogene-induced senescence.
19 ion of premalignant lesions is restrained by oncogene-induced senescence.
20 of HLX1 extends cellular lifespan and blunts oncogene-induced senescence.
21 ed the importance of the p38 MAPK pathway in oncogene-induced senescence.
22 3B protein are refractory to replicative and oncogene-induced senescence.
23 ion of H-Ras(V12), demonstrating its role in oncogene-induced senescence.
24 notypes reminiscent of those associated with oncogene-induced senescence.
25 r growth in BRAF-driven melanoma by inducing oncogene-induced senescence, a finding that might be exp
26 cription factor potently up-regulated during oncogene-induced senescence, a setting where it acts in
27  primary cells, mutant Ras instead can cause oncogene-induced senescence, a tumor suppressor function
28                 EGFR overexpression triggers oncogene-induced senescence, accompanied by the inductio
29            NPM has been reported to suppress oncogene-induced senescence and apoptosis and may repres
30 ntigen 3A (EBNA3A) and EBNA3C (which inhibit oncogene-induced senescence and apoptosis).
31            Growth inhibition was mediated by oncogene-induced senescence and associated with increase
32  a senescence response that is distinct from oncogene-induced senescence and can be targeted for canc
33 tion is a key requirement for replicative or oncogene-induced senescence and constitutes an important
34      Our results reveal diverse pathways for oncogene-induced senescence and further suggest that leu
35  status depicts a significant association of oncogene-induced senescence and g-protein activation pat
36   We also apply snapTotal-seq to profile the oncogene-induced senescence and identify the key regulat
37 domains (LADs) in replicative senescence and oncogene-induced senescence and overlap DNA hypomethylat
38  promoter of breast cancer that can overcome oncogene-induced senescence and reveal a selective vulne
39                         These two processes, oncogene-induced senescence and telomere-based crisis, e
40 ssion and thus the critical decision between oncogene-induced senescence and tumor initiation.
41 ve defined a signaling pathway that mediates oncogene-induced senescence, and identified posttranslat
42 , in terms of sensitivity to spontaneous and oncogene-induced senescence, and the R24P variant has li
43 c Runx-induced senescence contrasts with Ras oncogene-induced senescence, as it occurs directly and l
44 wever, elevated SUV420H2/H4K20me3 reinforces oncogene-induced senescence-associated proliferation arr
45 stent expression of BRAF(V600E) do not enter oncogene-induced senescence, but instead survive despite
46 C/EBPbeta has been shown to be necessary for oncogene-induced senescence, but the specific isoform of
47 e ERK2-DBP mutation attenuated JAK2-mediated oncogene-induced senescence by preventing the physical i
48                                              Oncogene-induced senescence causes hepatocytes to secret
49 intriguing how benign nevus cells can escape oncogene-induced senescence for malignant transformation
50                                              Oncogene-induced senescence has been shown to play a rol
51  tumor initiation and promotion by mediating oncogene-induced senescence in a murine skin carcinogene
52 se-associated protein SIN3B is essential for oncogene-induced senescence in cultured cells.
53 view builds upon the canonical hypothesis of oncogene-induced senescence in growth arrest and tumor s
54 Here, we show that depletion of Pak2 delayed oncogene-induced senescence in IMR90 human fibroblasts a
55        Hyperactivation of Ras is linked with oncogene-induced senescence in many cell types.
56 tumor suppressor MEN1 as a gene required for oncogene-induced senescence in melanocytes, raising the
57 ent observations have challenged the role of oncogene-induced senescence in melanocytic nevus formati
58  work, p15 represented a primary effector of oncogene-induced senescence in nevomelanocytes that was
59 thway through which oncogenic K-Ras promotes oncogene-induced senescence in normal cells while fuelin
60 ted RAS-induced lamin B1 loss and attenuates oncogene-induced senescence in primary human cells.
61 genic JAK2 kinase (JAK2V617F) from promoting oncogene-induced senescence in vitro.
62 hibition of signaling pathways implicated in oncogene-induced senescence including ATM/ATR and MAPK d
63 nt proliferation, while allowing escape from oncogene-induced senescence, independently of the oncoge
64                                      Such an oncogene-induced senescence involves activation of tumor
65                                              Oncogene induced senescence is a tumor suppressing defen
66                              Like apoptosis, oncogene-induced senescence is a barrier to tumor develo
67                                Subversion of oncogene-induced senescence is a key step during cancer
68                                              Oncogene-induced senescence is a mechanism of tumor supp
69                                              Oncogene-induced senescence is a tumor-suppressive defen
70                                              Oncogene-induced senescence is an anti-proliferative str
71                                              Oncogene-induced senescence is an important mechanism by
72                                              Oncogene-induced senescence is an important tumor-suppre
73                                              Oncogene-induced senescence is classically considered a
74 ced senescence, which implies that bypass of oncogene-induced senescence is necessary for malignant t
75                                          How oncogene-induced senescence is overcome during melanoma
76                                              Oncogene-induced senescence is thought to be invariably
77 pite the presence of markers associated with oncogene-induced senescence, low-grade PanIN were highly
78 catenin, and distinct from that of classical oncogene-induced senescence mediated by the well-known p
79 controls high-order chromatin networks in an oncogene-induced senescence model.
80 XCR2 (IL8RB) alleviates both replicative and oncogene-induced senescence (OIS) and diminishes the DNA
81 sion and telomere shortening, referred to as oncogene-induced senescence (OIS) and replicative senesc
82 hors demonstrated that RelA is a mediator of oncogene-induced senescence (OIS) and the senescence-ass
83                                              Oncogene-induced senescence (OIS) and therapy-induced se
84                                              Oncogene-induced senescence (OIS) can occur in response
85                                              Oncogene-induced senescence (OIS) constitutes a failsafe
86                       In normal human cells, oncogene-induced senescence (OIS) depends on induction o
87                                              Oncogene-induced senescence (OIS) is a critical tumor-su
88                                              Oncogene-induced senescence (OIS) is a potent tumor supp
89                                              Oncogene-induced senescence (OIS) is a stable cell cycle
90                                              Oncogene-induced senescence (OIS) is a tumor-suppressive
91                                              Oncogene-induced senescence (OIS) is an inherent and imp
92                                              Oncogene-induced senescence (OIS) is considered a powerf
93                                     Although oncogene-induced senescence (OIS) is considered a tumor
94        Tumor suppression that is mediated by oncogene-induced senescence (OIS) is considered to funct
95                                              Oncogene-induced senescence (OIS) is one form of senesce
96                     During tumor initiation, oncogene-induced senescence (OIS) is proposed to limit t
97                                              Oncogene-induced senescence (OIS) is thought to be a bar
98 els indicates that these mutations result in oncogene-induced senescence (OIS) of intestinal crypt ce
99                    C/EBPbeta is required for oncogene-induced senescence (OIS) of primary fibroblasts
100                                              Oncogene-induced senescence (OIS) protects normal cells
101 has been reported to increase, leading to an oncogene-induced senescence (OIS) response.
102 lls induces a permanent growth arrest called oncogene-induced senescence (OIS) that serves as a fail-
103 rounded by heavy lymphocyte infiltration and oncogene-induced senescence (OIS) was demonstrated by st
104                                              Oncogene-induced senescence (OIS) was triggered in a sub
105  cancers, and its overactivation can lead to oncogene-induced senescence (OIS), a barrier to cellular
106 a-catenin induces DNA damage, growth arrest, oncogene-induced senescence (OIS), and apoptosis of imma
107 from intestinal cells, thymocytes experience oncogene-induced senescence (OIS), growth arrest and apo
108                                       During oncogene-induced senescence (OIS), heterochromatin is lo
109                                              Oncogene-induced senescence (OIS), the proliferative arr
110 e depletion of which is sufficient to escape oncogene-induced senescence (OIS), thereby facilitating
111                           Since Hsf1 affects oncogene-induced senescence (OIS), these findings sugges
112 igger reactive cellular senescence, known as oncogene-induced senescence (OIS)-a putative autonomous
113 nction in telomere-induced, replicative, and oncogene-induced senescence (OIS).
114 ion, primary human and mouse cells can enter oncogene-induced senescence (OIS).
115 entering replicative senescence (RS) or upon oncogene-induced senescence (OIS).
116       C/EBPbeta is an important regulator of oncogene-induced senescence (OIS).
117 llular proliferation and ultimately triggers oncogene-induced senescence (OIS).
118  where it is required for the suppression of oncogene-induced senescence (OIS).
119 ostate and pancreatic cancers by suppressing oncogene-induced senescence (OIS).
120  that counteracts cellular transformation is oncogene-induced senescence (OIS).
121 implicated in Ras-induced transformation and oncogene-induced senescence (OIS).
122 ractivation or tumor suppressor dysfunction [oncogene-induced senescence (OIS)].
123 , implying that they are growth arrested via oncogene-induced senescence pathways.
124  in Her2-induced tumorigenesis by regulating oncogene-induced senescence pathways.
125 y, p16 functions as an essential mediator of oncogene-induced senescence preventing progression to me
126 strict melanoma progression by executing the oncogene-induced senescence program in benign nevi.
127 or number, size, burden and grade, bypass of oncogene-induced senescence, progression from adenoma to
128                The involvement of the DDR in oncogene-induced senescence prompted us to investigate t
129      Considerable data support the idea that oncogene-induced senescence remains a barrier that needs
130                                       During oncogene-induced senescence there are striking changes i
131  human fibroblasts undergoing replicative or oncogene-induced senescence, there is a marked decline i
132                             It also triggers oncogene-induced senescence to block Ras mutation.
133                  Our study demonstrates that oncogene-induced senescence triggered by a combination o
134 ng replicative senescence, Ndy1 inhibits Ras oncogene-induced senescence via a similar molecular mech
135 , persistent BRAF(V600E) expression triggers oncogene-induced senescence, which implies that bypass o
136                      Studies have shown that oncogene-induced senescence, which provides a barrier to
137 Precursor lesions with AGO2 ablation undergo oncogene-induced senescence with altered microRNA expres
138 icted to this pathway as a strategy to evade oncogene-induced senescence, with implications that inhi

 
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