ライフサイエンスコーパス: cigarette smoke condensate

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1 ively modulated by exogenous stimuli such as cigarette smoke condensate.

2 -1beta, PMA, LPS, H(2)O(2), doxorubicin, and cigarette smoke condensate.

3 cetate, okadaic acid, hydrogen peroxide, and cigarette smoke condensate also was suppressed.

4 agent, referred to as CSC, was isolated from cigarette smoke condensate and shown to prime purified h

5 orbol 12-myristate 13-acetate, H(2)O(2), and cigarette smoke condensate as well as that induced by TN

6 In mice, paternal exposure to cigarette smoke condensate (CSC) causes molecular defect

7 ere cultured in normal media with or without cigarette smoke condensate (CSC) for up to 9 months unde

8 Cigarette smoke condensate (CSC) is comprised of thousan

9 Cigarette smoke condensate (CSC) is the particulate matt

10 that exposure of esophageal cancer cells to cigarette smoke condensate (CSC) led to upregulation of

11 d the effect of hydrogen peroxide (H2O2) and cigarette smoke condensate (CSC) on histone acetylation:

12 In this study, we investigated the effect of cigarette smoke condensate (CSC) on the characteristics

13 f pregnant p(un) mice to cigarette smoke and cigarette smoke condensate (CSC) on the frequency of bla

14 Following exposure to carcinogens: cigarette smoke condensate (CSC) or N-nitrosamine-4-(met

15 epithelial cell line, MCF10A, for 72 h with cigarette smoke condensate (CSC) resulted in a transform

16 vious studies have shown that treatment with cigarette smoke condensate (CSC) transforms normal breas

17 In earlier studies, we have shown that cigarette smoke condensate (CSC), a surrogate for cigare

18 d in primary bronchial epithelium exposed to cigarette smoke condensate (CSC), and alteration of mir-

19 (NHBE) resulted in significant inhibition of cigarette smoke condensate (CSC)-induced cell proliferat

20 ng adenocarcinoma H1299 cells, we found that cigarette smoke condensate (CSC)-induced NF-kappaB activ

21 lls cultured in normal media with or without cigarette smoke condensate (CSC).

22 cells cultured in the presence or absence of cigarette smoke condensate (CSC).

23 cells exhibit similar molecular responses to cigarette smoke condensate ex vivo and in vivo.

24 The neutral fraction of cigarette smoke condensate had most of the carcinogenic

25 s factor (TNF), phorbol ester, okadaic acid, cigarette smoke condensate, hydrogen peroxide, and inter

26 rom immortalized HBE cells after exposure to cigarette smoke condensate in vivo.

27 A549 cell exposure to cigarette smoke condensate increased these enhancer mark

28 (e.g. phorbol 12-myristate 13-acetate, H2O2, cigarette smoke condensate, interleukin-1beta, lipopolys

29 It was concluded from these studies that cigarette smoke condensate is primarily a tumor-promotin

30 sate were also performed, and indicated that cigarette smoke condensate leads to genome instability i

31 arcinogenic and inflammatory agents, such as cigarette smoke condensate, phorbol 12-myristate 13-acet

32 y tumor necrosis factor (TNF), okadaic acid, cigarette smoke condensate, phorbol myristate acetate, a

33 benzo[a]pyrene (BaP) is a major component of cigarette smoke condensate that has received significant

34 pressed NF-kappaB activated by a carcinogen (cigarette smoke condensate), tumor promoters (phorbol my

35 by lipopolysaccharide, interleukin-1beta, or cigarette smoke condensate was completely suppressed in

36 bronchial epithelial cell lines treated with cigarette smoke condensate were also performed, and indi

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