ライフサイエンスコーパス: chemical carcinogenesis

1 formation of nonmelanoma skin tumors during chemical carcinogenesis.

2 xhibit more highly aggressive HCC induced by chemical carcinogenesis.

3 epidermis exhibit increased vulnerability to chemical carcinogenesis.

4 fferentiation in the ears of Dsk5 mice after chemical carcinogenesis.

5 nslational receptor down-regulation, to skin chemical carcinogenesis.

6 lagen VII hypomorphic mouse model of RDEB to chemical carcinogenesis.

7 cells (IMCs) that are recruited early on in chemical carcinogenesis.

8 genic signals and plays an essential role in chemical carcinogenesis.

9 insults, including electrophile attacks and chemical carcinogenesis.

10 it is believed to play an important role in chemical carcinogenesis.

11 ion of DNA adducts have been associated with chemical carcinogenesis.

12 d accelerating invasion and metastasis after chemical carcinogenesis.

13 to confer complete resistance of the skin to chemical carcinogenesis.

14 el) to determine the in vivo role of NQO2 in chemical carcinogenesis.

15 ocarcinogens, indicating a potential role in chemical carcinogenesis.

16 obably does not play a physiological role in chemical carcinogenesis.

17 ) or TNFR2 (TNFR2-/- mice) were subjected to chemical carcinogenesis.

18 version stage in a clonal epidermal model of chemical carcinogenesis.

19 seen in hepatocellular carcinomas induced by chemical carcinogenesis.

20 of skin tumorigenesis that did not rely upon chemical carcinogenesis.

21 ich may reflect individual susceptibility to chemical carcinogenesis.

22 tion presented here may aid in understanding chemical carcinogenesis and cancer recurrence after chem

23 into the epigenetic regulation of viral vs. chemical carcinogenesis and could provide novel targets

24 Herein we use a mouse model of primary chemical carcinogenesis and demonstrate that equilibrium

25 us cell carcinoma used for investigations of chemical carcinogenesis and for the evaluation of putati

26 Critical to mechanisms of chemical carcinogenesis and the design of chemopreventiv

27 gate the role of these proteins in cutaneous chemical carcinogenesis and to determine whether their e

28 tories on the effects of enzyme induction on chemical carcinogenesis as an approach to cancer chemopr

29 During chemical carcinogenesis, both transgenes increased papil

30 A key question in chemical carcinogenesis by metabolically activated polyc

31 During two-stage mouse skin chemical carcinogenesis, CD151 reduces tumor lag time an

32 Nrf2 responses provide protection against chemical carcinogenesis, chronic inflammation, neurodege

33 In two-stage chemical carcinogenesis experiments using DMBA as the tu

34 mouse significantly heightens sensitivity to chemical carcinogenesis, growth of transplanted tumors,

35 y, microbiology, virology, environmental and chemical carcinogenesis, immunology, pathology, molecula

36 A number of isothiocyanates block chemical carcinogenesis in a variety of animal models by

37 We used the murine skin model of chemical carcinogenesis in genetic linkage analysis of t

38 eotide excision repair in protection against chemical carcinogenesis in internal organs, we treated X

39 in of function during multistage murine skin chemical carcinogenesis in K14-HIF-1alpha(Pro402A564G) (

40 erase mediated DNA repair effectively blocks chemical carcinogenesis in mice carrying the LMO1 oncoge

41 Chemical carcinogenesis in mouse skin has been useful in

42 apillomas and carcinomas following two-stage chemical carcinogenesis in skin.

43 itic cell (DC), are protected from cutaneous chemical carcinogenesis, independent of T cell immunity.

44 theory of the origin of cancer-field theory, chemical carcinogenesis, infection, mutation, or epigene

45 T cell deficiency can increase resistance to chemical carcinogenesis initiated by 7,12-dimethylbenz[a

46 Using a chemical carcinogenesis model in Sparc-deficient mice an

47 on tumor development in the murine multistep chemical carcinogenesis model of squamous cell carcinoma

48 s, murine papilloma formation in a classical chemical carcinogenesis model was reduced in DEK knockou

49 plus phorbol myristate acetate-induced skin chemical carcinogenesis model, acute dosing of establish

50 rotected against developing lung tumors in a chemical carcinogenesis model.

51 on skin tumor development using the 2-stage chemical carcinogenesis model.

52 hance carcinoma development in an epithelial chemical carcinogenesis model.

53 n immature and point to a continued need for chemical carcinogenesis models to screen for the potenti

54 In chemical carcinogenesis models, GRP94 (gp96) elicits tum

55 this contributes to cancer, we did two-stage chemical carcinogenesis on K14DeltaNLef1 transgenic mice

56 d-type and MMP-3 null mice were subjected to chemical carcinogenesis procedures by topical applicatio

57 When subjected to a two-stage chemical carcinogenesis protocol (dimethylbenz[alpha]ant

58 On this classic chemical carcinogenesis protocol, DKO mice showed a sign

59 mice were subjected to a standard two-stage chemical carcinogenesis protocol, they exhibited an incr

60 These mice were exposed to a chemical carcinogenesis protocol, which allows tumorigen

61 d an increased susceptibility to a two-stage chemical carcinogenesis protocol, with the rate of forma

62 uamous cell carcinoma (SCC) development in a chemical carcinogenesis protocol.

63 (WT) mice were subjected to a two-stage skin chemical carcinogenesis protocol.

64 o cutaneous tumor development in response to chemical carcinogenesis protocols and, remarkably, that

65 ice exhibited an increased susceptibility to chemical carcinogenesis protocols at both early and late

66 PCC cell lines and primary tumors induced by chemical carcinogenesis protocols, thus implicating this

67 y more susceptible than LC-deficient mice to chemical carcinogenesis provoked by initiation with the

68 ntly increased the susceptibility of mice to chemical carcinogenesis, resulting in development of squ

69 To investigate the role of NQO1 in chemical carcinogenesis, the dorsal skin of NQO1-deficie

70 one of the two primary carcinogenic routes: chemical carcinogenesis through exposure to tobacco and

71 study, we used an established mouse model of chemical carcinogenesis to investigate how 1,25-VD preve

72 Thus, tissue-associated DC can enhance chemical carcinogenesis via PAH metabolism, highlighting