ライフサイエンスコーパス: PUVA

1 PUVA exerts its antiproliferative activity through forma

2 Among patients with <100 PUVA treatments, high UVB exposure was significantly ass

3 n is close to that recorded for at least 200 PUVA treatments (3.1 [2.6-3.7] and 2.8 [2.6-3.2], respec

4 her among patients who received at least 250 PUVA treatments than among those who received fewer trea

5 five (80%) skin warts, and four of 12 (33%) PUVA-exposed normal skin samples.

6 The results indicated that 10 of 13 (77%) PUVA-induced skin tumors contained missense mutations pr

7 Sunlight and psoralen and ultraviolet A (PUVA) are risk factors for the development of squamous c

8 traviolet radiation, psoralen-ultraviolet A (PUVA), and topical drugs used to treat psoriasis.

9 The Psoralen plus Ultraviolet-A (PUVA) cohort study has been a tremendous success in dete

10 In contrast, tumor-adjacent, PUVA-exposed skin from tumor-bearing animals did not exh

11 cyls in all major phospholipid classes after PUVA.

12 site-specificities were more prevalent after PUVA-II treatment.

13 -neighboring side, was more pronounced after PUVA-II treatment.

14 ively followed 1380 patients who first began PUVA treatment for psoriasis in 1975-1976.

15 s concern about possible association between PUVA treatment and an increased risk of noncutaneous can

16 A-I treatment and subsequently, augmented by PUVA-II treatment, leaving a unique mutational signature

17 Since the DNA damage induced by PUVA is quite different from that induced by UV, we inve

18 sensor and alpha-synuclein was inhibited by PUVA.

19 hat PUVA-induced mutagenesis is initiated by PUVA-I treatment and subsequently, augmented by PUVA-II

20 vation was furthermore affected similarly by PUVA following PAR1 (effective half-maximal concentratio

21 The characteristic PUVA-induced mutations predominate in the p53 mutational

22 In conclusion, PUVA increases the order of lipid phases by covalent mod

23 ependent treatment of certain skin diseases (PUVA therapy).

24 trolled in vivo test systems or in high-dose PUVA-treated patients, and also are easily recognizable

25 ts treated with a single or split PUVA dose (PUVA-I or PUVA-II, respectively).

26 skin cancer, seven of 17 (41.2%) dysplastic PUVA keratoses, four of five (80%) skin warts, and four

27 including in normal skin, warts, dysplastic PUVA keratoses, and squamous cell carcinomas.

28 in determining how a novel treatment (i.e., PUVA) affects the long-term risk of keratinocyte carcino

29 We also analysed the entire PUVA study cohort (1380) to assess the relation between

30 e of HPV infection in cutaneous lesions from PUVA-treated patients is similar to that previously repo

31 However, PUVA is mutagenic, increases the risk of squamous-cell s

32 However, PUVA treatment increases the risk of developing skin can

33 nd II patients were evaluable: 40 in the IFN+PUVA group and 42 in the IFN+acitretin group.

34 With 70% complete remissions in the IFN+PUVA group, this treatment was significantly superior to

35 esponse was significantly shorter in the IFN+PUVA group, with 18.6 weeks compared with 21.8 weeks in

36 s to basal cell carcinoma ratio (SCC:BCC) in PUVA-treated patients, also seen in immunosuppressed ren

37 signature" mutations were rarely detected in PUVA-induced skin cancers, we can conclude that PUVA act

38 esions, and suggests that the role of HPV in PUVA-associated carcinogenesis merits further study.

39 Interestingly, about 40% of all mutations in PUVA-induced skin tumors occurred at 5'-TA sites, and an

40 iscernible in the p53 mutational spectrum in PUVA-treated patients but complex exposure to other ther

41 ge induced by psoralen plus UVA irradiation (PUVA) or UVC radiation, showing less survival and increa

42 exposed to psoralen and ultraviolet-A light (PUVA) and other treatments for severe psoriasis.

43 Psoralen and ultraviolet A light (PUVA) are used to kill pathogens in blood products and a

44 Psoralen plus UVA light (PUVA) is commonly used to treat psoriasis, a common skin

45 is well described, but the direct effects of PUVA on cell signal transduction are poorly understood.

46 The signature mutations of PUVA are discernible in the p53 mutational spectrum in P

47 e first treatment and with a large number of PUVA treatments (> or = 250).

48 ome sunscreens and which are used as part of PUVA (psoralens and ultraviolet-A) photochemotherapy tre

49 To investigate the etiological relevance of PUVA for these diseases, we performed mutation spectrome

50 ects enrolled in a long-term safety trial of PUVA therapy.

51 with a single or split PUVA dose (PUVA-I or PUVA-II, respectively).

52 also are easily recognizable in the overall PUVA-treated patients.

53 inations of IFN with oral photochemotherapy (PUVA) or retinoids were investigated in nonrandomized tr

54 In platelets, PUVA caused poor membrane binding of Akt and Bruton's ty

55 hese two combination therapies, ie, IFN plus PUVA and IFN plus acitretin.

56 alen (psoralen) and ultraviolet A radiation (PUVA) is an effective treatment for psoriasis.

57 ion of psoralen and ultraviolet A radiation (PUVA) is widely used in the treatment of psoriasis.

58 ergoing psoralen plus ultraviolet radiation (PUVA) therapy are susceptible for squamous cell carcinom

59 Like ultraviolet B radiation, PUVA is both mutagenic and immunosuppressive and may thu

60 CYP2S1 was induced by ultraviolet radiation, PUVA, coal tar, and all-trans retinoic acid; expression

61 Since PUVA induces DNA cross-links exclusively at these sites

62 c fibroblasts treated with a single or split PUVA dose (PUVA-I or PUVA-II, respectively).

63 acorporeal photopheresis, a form of systemic PUVA.

64 es not support the hypothesis that long-term PUVA treatment increases the risk of noncutaneous cancer

65 A-induced skin cancers, we can conclude that PUVA acts as a carcinogen by inducing unique PUVA signat

66 We conclude that PUVA-induced mutagenesis is initiated by PUVA-I treatmen

67 Stern and Huibregtse report results from the PUVA follow-up study and conclude that only patients wit

68 rt crossover study of 28 participants in the PUVA follow-up study who were on ciclosporin to compare

69 ed with psoralens and ultraviolet-A therapy (PUVA) who enrolled in a cohort study in 1975-1976.

70 ents with psoriasis who have been exposed to PUVA.

71 oma and documented the extent of exposure to PUVA among 1380 patients with psoriasis who were first t

72 , after adjustment for amount of exposure to PUVA and methotrexate, incidence of tumours was seven ti

73 ciation between higher levels of exposure to PUVA and the risk of any of these cancers.

74 cer in psoriasis patients who have undergone PUVA therapy.

75 PUVA acts as a carcinogen by inducing unique PUVA signature mutations in p53.

76 Psoralen and UVA (PUVA) photochemotherapy is associated with a dose-depend

77 that induced by UV, we investigated whether PUVA-induced mouse skin cancers display carcinogen-speci

78 To better understand the mechanism by which PUVA treatment induces p53, we exposed human skin fibrob

79 p53, we exposed human skin fibroblasts with PUVA under conditions that differentially produce monoad

80 NMSC risk, much less than that observed with PUVA.

81 s with psoriasis who were first treated with PUVA in 1975 or 1976.

82 ence of melanoma among patients treated with PUVA.

83 bout 15 years after the first treatment with PUVA, the risk of malignant melanoma increases, especial