ライフサイエンスコーパス: oncogene-induced senescence

1 nd p38alpha contribute to MSK1 activation in oncogene-induced senescence.

2 n addition NR2E1 expression also counteracts oncogene-induced senescence.

3 ted by oncogenic stress, and is required for oncogene-induced senescence.

4 H1 loss provokes DNA damage and induction of oncogene-induced senescence.

5 RAS-induced DNA damage and thereby reinforce oncogene-induced senescence.

6 t remains unclear whether they can influence oncogene-induced senescence.

7 ally due to NF-kappaB-mediated abrogation of oncogene-induced senescence.

8 ivates UCA1, revealing a novel mechanism for oncogene-induced senescence.

9 ion of premalignant lesions is restrained by oncogene-induced senescence.

10 of HLX1 extends cellular lifespan and blunts oncogene-induced senescence.

11 e an irreversible cell cycle arrest known as oncogene-induced senescence.

12 ed the importance of the p38 MAPK pathway in oncogene-induced senescence.

13 3B protein are refractory to replicative and oncogene-induced senescence.

14 ion of H-Ras(V12), demonstrating its role in oncogene-induced senescence.

15 notypes reminiscent of those associated with oncogene-induced senescence.

16 an tumors, and show coincident regulation in oncogene-induced senescence.

17 r growth in BRAF-driven melanoma by inducing oncogene-induced senescence, a finding that might be exp

18 cription factor potently up-regulated during oncogene-induced senescence, a setting where it acts in

19 primary cells, mutant Ras instead can cause oncogene-induced senescence, a tumor suppressor function

20 EGFR overexpression triggers oncogene-induced senescence, accompanied by the inductio

21 NPM has been reported to suppress oncogene-induced senescence and apoptosis and may repres

22 ntigen 3A (EBNA3A) and EBNA3C (which inhibit oncogene-induced senescence and apoptosis).

23 a senescence response that is distinct from oncogene-induced senescence and can be targeted for canc

24 tion is a key requirement for replicative or oncogene-induced senescence and constitutes an important

25 Our results reveal diverse pathways for oncogene-induced senescence and further suggest that leu

26 domains (LADs) in replicative senescence and oncogene-induced senescence and overlap DNA hypomethylat

27 These two processes, oncogene-induced senescence and telomere-based crisis, e

28 ssion and thus the critical decision between oncogene-induced senescence and tumor initiation.

29 ve defined a signaling pathway that mediates oncogene-induced senescence, and identified posttranslat

30 , in terms of sensitivity to spontaneous and oncogene-induced senescence, and the R24P variant has li

31 c Runx-induced senescence contrasts with Ras oncogene-induced senescence, as it occurs directly and l

32 wever, elevated SUV420H2/H4K20me3 reinforces oncogene-induced senescence-associated proliferation arr

33 stent expression of BRAF(V600E) do not enter oncogene-induced senescence, but instead survive despite

34 C/EBPbeta has been shown to be necessary for oncogene-induced senescence, but the specific isoform of

35 Oncogene-induced senescence causes hepatocytes to secret

36 intriguing how benign nevus cells can escape oncogene-induced senescence for malignant transformation

37 Oncogene-induced senescence has been shown to play a rol

38 tumor initiation and promotion by mediating oncogene-induced senescence in a murine skin carcinogene

39 se-associated protein SIN3B is essential for oncogene-induced senescence in cultured cells.

40 view builds upon the canonical hypothesis of oncogene-induced senescence in growth arrest and tumor s

41 Hyperactivation of Ras is linked with oncogene-induced senescence in many cell types.

42 tumor suppressor MEN1 as a gene required for oncogene-induced senescence in melanocytes, raising the

43 work, p15 represented a primary effector of oncogene-induced senescence in nevomelanocytes that was

44 ted RAS-induced lamin B1 loss and attenuates oncogene-induced senescence in primary human cells.

45 hibition of signaling pathways implicated in oncogene-induced senescence including ATM/ATR and MAPK d

46 Such an oncogene-induced senescence involves activation of tumor

47 Like apoptosis, oncogene-induced senescence is a barrier to tumor develo

48 Subversion of oncogene-induced senescence is a key step during cancer

49 Oncogene-induced senescence is a mechanism of tumor supp

50 Oncogene-induced senescence is a tumor-suppressive defen

51 Oncogene-induced senescence is an anti-proliferative str

52 Oncogene-induced senescence is an important mechanism by

53 Oncogene-induced senescence is an important tumor-suppre

54 Oncogene-induced senescence is classically considered a

55 ced senescence, which implies that bypass of oncogene-induced senescence is necessary for malignant t

56 How oncogene-induced senescence is overcome during melanoma

57 Oncogene-induced senescence is thought to be invariably

58 pite the presence of markers associated with oncogene-induced senescence, low-grade PanIN were highly

59 catenin, and distinct from that of classical oncogene-induced senescence mediated by the well-known p

60 XCR2 (IL8RB) alleviates both replicative and oncogene-induced senescence (OIS) and diminishes the DNA

61 hors demonstrated that RelA is a mediator of oncogene-induced senescence (OIS) and the senescence-ass

62 Oncogene-induced senescence (OIS) and therapy-induced se

63 Oncogene-induced senescence (OIS) can occur in response

64 Oncogene-induced senescence (OIS) constitutes a failsafe

65 In normal human cells, oncogene-induced senescence (OIS) depends on induction o

66 Oncogene-induced senescence (OIS) is a critical tumor-su

67 Oncogene-induced senescence (OIS) is a potent tumor supp

68 Oncogene-induced senescence (OIS) is a tumor-suppressive

69 Oncogene-induced senescence (OIS) is considered a powerf

70 Although oncogene-induced senescence (OIS) is considered a tumor

71 Tumor suppression that is mediated by oncogene-induced senescence (OIS) is considered to funct

72 During tumor initiation, oncogene-induced senescence (OIS) is proposed to limit t

73 Oncogene-induced senescence (OIS) is thought to be a bar

74 els indicates that these mutations result in oncogene-induced senescence (OIS) of intestinal crypt ce

75 C/EBPbeta is required for oncogene-induced senescence (OIS) of primary fibroblasts

76 Oncogene-induced senescence (OIS) protects normal cells

77 has been reported to increase, leading to an oncogene-induced senescence (OIS) response.

78 lls induces a permanent growth arrest called oncogene-induced senescence (OIS) that serves as a fail-

79 rounded by heavy lymphocyte infiltration and oncogene-induced senescence (OIS) was demonstrated by st

80 a-catenin induces DNA damage, growth arrest, oncogene-induced senescence (OIS), and apoptosis of imma

81 from intestinal cells, thymocytes experience oncogene-induced senescence (OIS), growth arrest and apo

82 Oncogene-induced senescence (OIS), the proliferative arr

83 e depletion of which is sufficient to escape oncogene-induced senescence (OIS), thereby facilitating

84 Since Hsf1 affects oncogene-induced senescence (OIS), these findings sugges

85 C/EBPbeta is an important regulator of oncogene-induced senescence (OIS).

86 ion, primary human and mouse cells can enter oncogene-induced senescence (OIS).

87 llular proliferation and ultimately triggers oncogene-induced senescence (OIS).

88 where it is required for the suppression of oncogene-induced senescence (OIS).

89 ostate and pancreatic cancers by suppressing oncogene-induced senescence (OIS).

90 that counteracts cellular transformation is oncogene-induced senescence (OIS).

91 implicated in Ras-induced transformation and oncogene-induced senescence (OIS).

92 , implying that they are growth arrested via oncogene-induced senescence pathways.

93 in Her2-induced tumorigenesis by regulating oncogene-induced senescence pathways.

94 y, p16 functions as an essential mediator of oncogene-induced senescence preventing progression to me

95 strict melanoma progression by executing the oncogene-induced senescence program in benign nevi.

96 or number, size, burden and grade, bypass of oncogene-induced senescence, progression from adenoma to

97 The involvement of the DDR in oncogene-induced senescence prompted us to investigate t

98 Considerable data support the idea that oncogene-induced senescence remains a barrier that needs

99 human fibroblasts undergoing replicative or oncogene-induced senescence, there is a marked decline i

100 It also triggers oncogene-induced senescence to block Ras mutation.

101 Our study demonstrates that oncogene-induced senescence triggered by a combination o

102 ng replicative senescence, Ndy1 inhibits Ras oncogene-induced senescence via a similar molecular mech

103 , persistent BRAF(V600E) expression triggers oncogene-induced senescence, which implies that bypass o

104 Studies have shown that oncogene-induced senescence, which provides a barrier to

105 icted to this pathway as a strategy to evade oncogene-induced senescence, with implications that inhi