ライフサイエンスコーパス: photocarcinogenesis

1 vents immune suppression and interferes with photocarcinogenesis.

2 nase-2 (Cox-2), and Cox-2 inhibition reduces photocarcinogenesis.

3 pproaches are desired to effectively prevent photocarcinogenesis.

4 this growth signaling pathway contributes to photocarcinogenesis.

5 o the observed ability of T-oligos to reduce photocarcinogenesis.

6 vely deleted to examine the role of COX-1 in photocarcinogenesis.

7 oxib, to suppress hyperemia formation during photocarcinogenesis.

8 lar mechanisms of silibinin efficacy against photocarcinogenesis.

9 by UV radiation is a critical event in skin photocarcinogenesis.

10 xygen species contributing to photoaging and photocarcinogenesis.

11 nocytes, we studied the role of this gene in photocarcinogenesis.

12 nitive role of ODC in the promotion phase of photocarcinogenesis.

13 s a model of immunologic events occurring in photocarcinogenesis.

14 be effective in preventing solar UVR-induced photocarcinogenesis.

15 cytes which protects against photodamage and photocarcinogenesis.

16 useful model for the study of acute exposure photocarcinogenesis.

17 mmune responses, and thus may play a role in photocarcinogenesis.

18 d mice, suggesting involvement of cis-UCA in photocarcinogenesis.

19 nm) in dermal inflammation, photoaging, and photocarcinogenesis.

20 oimmunosuppression with a consequent role in photocarcinogenesis.

21 Risk estimates based on the human photocarcinogenesis action spectrum predict that narrowb

22 Photocarcinogenesis and photoaging are established conse

23 g ultraviolet A (315-400 nm) (UVA) may cause photocarcinogenesis and photoaging.

24 Here, we show that agents known to reverse photocarcinogenesis and photoimmune suppression, such as

25 e most common and highly sensitive model for photocarcinogenesis, and in littermate nontransgenic mic

26 rmal hyperplasia, oxidative skin damage, and photocarcinogenesis as compared to wild type mice.

27 eptible to both UVB-induced inflammation and photocarcinogenesis because of the deficiency in the rep

28 e stress underlying cutaneous photoaging and photocarcinogenesis, but the molecular identity of non-D

29 is previously unreported that prevention of photocarcinogenesis by GTPs is mediated through IL-12-de

30 ccurring during the tumor promotion phase of photocarcinogenesis could lead to the development of nov

31 a bioactive phytochemical, strongly prevents photocarcinogenesis; however, its mechanism is not fully

32 udy, we tested the ability of POH to inhibit photocarcinogenesis in a nonmelanoma model of mouse skin

33 entosum C (Xpc) gene, will heighten melanoma photocarcinogenesis in an Ink4a-Arf-deficient background

34 Topically administered alpha-TH prevents UVB photocarcinogenesis in C3H mice, whereas alpha-TAc does

35 two major mechanisms underlie the increased photocarcinogenesis in fair/light skin.

36 bility, we determined the effects of EGCG on photocarcinogenesis in IL-12 knockout (KO) mice using th

37 e and tumor multiplicity but did not prevent photocarcinogenesis in IL-12 KO mice.

38 X1 activation leads to evidence of decreased photocarcinogenesis in in vitro keratinocytes and in wel

39 IL-12 deficiency has been shown to promote photocarcinogenesis in mice.

40 s deficiency of interleukin (IL)-12 promotes photocarcinogenesis in mice.

41 the major polyphenol of green tea, prevents photocarcinogenesis in mice.

42 genase (COX-2), and COX-2 inhibition reduces photocarcinogenesis in mice.

43 olyphenols (GTPs) in drinking water prevents photocarcinogenesis in mice; however, the molecular mech

44 ls and decrease UV-induced mutation rate and photocarcinogenesis in mouse skin.

45 treatment caused a strong protection against photocarcinogenesis in terms of delay in tumor appearanc

46 decreases UV-induced mutations, and reduces photocarcinogenesis in UV-irradiated hairless WT repair-

47 lication of EGCG (1 mg/cm(2) skin) prevented photocarcinogenesis in wild-type (C3H/HeN) mice in terms

48 ding resulted in a strong protection against photocarcinogenesis, in terms of tumor multiplicity (60-

49 Photocarcinogenesis, like other cancers, is a multistep

50 ermal melanocytes is critical for inhibiting photocarcinogenesis, particularly melanoma, the most dea

51 eveloped into topical agents to prevent skin photocarcinogenesis, particularly melanoma.

52 h Ink4a-Arf inactivation, can drive melanoma photocarcinogenesis possibly through signature Kras muta

53 extent of EP(1) involvement in the cutaneous photocarcinogenesis process is unknown.

54 ir wild-type counterparts and an established photocarcinogenesis protocol, we found that although adm

55 d-type (WT) counterparts were subjected to a photocarcinogenesis protocol.

56 r wild-type counterparts were subjected to a photocarcinogenesis protocol; skin and tumor samples wer

57 ls may play a critical role in the decreased photocarcinogenesis seen in individuals with darker skin

58 In contrast to other mouse stains used in photocarcinogenesis studies, few p53 mutations were foun

59 ate for the first time that EGCG can prevent photocarcinogenesis through an EGCG-induced IL-12-depend

60 sibility that EGCG also prevents UVB-induced photocarcinogenesis through an IL-12-dependent DNA repai

61 se against UVB-induced skin inflammation and photocarcinogenesis through elevated activation of Nrf2

62 violet B (UVB)-induced skin inflammation and photocarcinogenesis using hairless fat-1 transgenic mice

63 MCGA3 could be a useful agent to prevent photocarcinogenesis via apoptotic elimination of p53 mut

64 in causes a strong protective effect against photocarcinogenesis via down-regulation of inflammatory

65 As immunosuppression is a risk factor for photocarcinogenesis, we investigated the possibility tha

66 ong preventive efficacy of silibinin against photocarcinogenesis, which involves the inhibition of DN