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1 of skin tumorigenesis that did not rely upon chemical carcinogenesis.
2 epidermis exhibit increased vulnerability to chemical carcinogenesis.
3 ical roles of the METTL3-m(6)A-CDCP1 axis in chemical carcinogenesis.
4 fferentiation in the ears of Dsk5 mice after chemical carcinogenesis.
5 nslational receptor down-regulation, to skin chemical carcinogenesis.
6  cells (IMCs) that are recruited early on in chemical carcinogenesis.
7 genic signals and plays an essential role in chemical carcinogenesis.
8  insults, including electrophile attacks and chemical carcinogenesis.
9  formation of nonmelanoma skin tumors during 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 xhibit more highly aggressive HCC induced by chemical carcinogenesis.
15 el) to determine the in vivo role of NQO2 in chemical carcinogenesis.
16 ocarcinogens, indicating a potential role in chemical carcinogenesis.
17 obably does not play a physiological role in chemical carcinogenesis.
18 ) or TNFR2 (TNFR2-/- mice) were subjected to chemical carcinogenesis.
19 lagen VII hypomorphic mouse model of RDEB to chemical carcinogenesis.
20 version stage in a clonal epidermal model of chemical carcinogenesis.
21 seen in hepatocellular carcinomas induced by chemical carcinogenesis.
22 ich may reflect individual susceptibility to chemical carcinogenesis.
23 he prevention of photocarcinogenesis but not chemical carcinogenesis.
24 tion presented here may aid in understanding chemical carcinogenesis and cancer recurrence after chem
25  into the epigenetic regulation of viral vs. chemical carcinogenesis and could provide novel targets
26       Herein we use a mouse model of primary chemical carcinogenesis and demonstrate that equilibrium
27 us cell carcinoma used for investigations of chemical carcinogenesis and for the evaluation of putati
28 7-based therapy, we exposed K5.Smad7 skin to chemical carcinogenesis and found reduced myeloid leukoc
29                    Critical to mechanisms of chemical carcinogenesis and the design of chemopreventiv
30 gate the role of these proteins in cutaneous chemical carcinogenesis and to determine whether their e
31 one biosynthesis, lipid and atherosclerosis, chemical carcinogenesis, and pathways in cancer.
32 tories on the effects of enzyme induction on chemical carcinogenesis as an approach to cancer chemopr
33                                       During chemical carcinogenesis, both transgenes increased papil
34                            A key question in chemical carcinogenesis by metabolically activated polyc
35                  During two-stage mouse skin chemical carcinogenesis, CD151 reduces tumor lag time an
36    Nrf2 responses provide protection against chemical carcinogenesis, chronic inflammation, neurodege
37                                 In two-stage chemical carcinogenesis experiments using DMBA as the tu
38 mouse significantly heightens sensitivity to chemical carcinogenesis, growth of transplanted tumors,
39 y, microbiology, virology, environmental and chemical carcinogenesis, immunology, pathology, molecula
40            A number of isothiocyanates block chemical carcinogenesis in a variety of animal models by
41             We used the murine skin model of chemical carcinogenesis in genetic linkage analysis of t
42 eotide excision repair in protection against chemical carcinogenesis in internal organs, we treated X
43 in of function during multistage murine skin chemical carcinogenesis in K14-HIF-1alpha(Pro402A564G) (
44 erase mediated DNA repair effectively blocks chemical carcinogenesis in mice carrying the LMO1 oncoge
45                                              Chemical carcinogenesis in mouse skin has been useful in
46 apillomas and carcinomas following two-stage chemical carcinogenesis in skin.
47 itic cell (DC), are protected from cutaneous chemical carcinogenesis, independent of T cell immunity.
48 theory of the origin of cancer-field theory, chemical carcinogenesis, infection, mutation, or epigene
49 T cell deficiency can increase resistance to chemical carcinogenesis initiated by 7,12-dimethylbenz[a
50                                      Using a chemical carcinogenesis model in Sparc-deficient mice an
51 on tumor development in the murine multistep chemical carcinogenesis model of squamous cell carcinoma
52 s, murine papilloma formation in a classical chemical carcinogenesis model was reduced in DEK knockou
53  plus phorbol myristate acetate-induced skin chemical carcinogenesis model, acute dosing of establish
54 hance carcinoma development in an epithelial chemical carcinogenesis model.
55 rotected against developing lung tumors in a chemical carcinogenesis model.
56  on skin tumor development using the 2-stage chemical carcinogenesis model.
57 FD) and recorded mammary tumor outcomes in a chemical carcinogenesis model.
58 n immature and point to a continued need for chemical carcinogenesis models to screen for the potenti
59                                           In chemical carcinogenesis models, GRP94 (gp96) elicits tum
60 ve bladder cancer (NMIBC) that ensued in the chemical carcinogenesis N-butyl-N-(4-hydroxybutyl)-nitro
61         PDV is a cSCC cell line derived from chemical carcinogenesis of mouse keratinocytes.
62                                              Chemical carcinogenesis of the stomach is associated wit
63 this contributes to cancer, we did two-stage chemical carcinogenesis on K14DeltaNLef1 transgenic mice
64 d-type and MMP-3 null mice were subjected to chemical carcinogenesis procedures by topical applicatio
65                When subjected to a two-stage chemical carcinogenesis protocol (dimethylbenz[alpha]ant
66                              On this classic chemical carcinogenesis protocol, DKO mice showed a sign
67  mice were subjected to a standard two-stage chemical carcinogenesis protocol, they exhibited an incr
68                 These mice were exposed to a chemical carcinogenesis protocol, which allows tumorigen
69 d an increased susceptibility to a two-stage chemical carcinogenesis protocol, with the rate of forma
70 uamous cell carcinoma (SCC) development in a chemical carcinogenesis protocol.
71 (WT) mice were subjected to a two-stage skin chemical carcinogenesis protocol.
72 o cutaneous tumor development in response to chemical carcinogenesis protocols and, remarkably, that
73 ice exhibited an increased susceptibility to chemical carcinogenesis protocols at both early and late
74 PCC cell lines and primary tumors induced by chemical carcinogenesis protocols, thus implicating this
75 y more susceptible than LC-deficient mice to chemical carcinogenesis provoked by initiation with the
76 s physiological events, the role of m(6)A in chemical carcinogenesis remains largely unknown.
77 ntly increased the susceptibility of mice to chemical carcinogenesis, resulting in development of squ
78           To investigate the role of NQO1 in chemical carcinogenesis, the dorsal skin of NQO1-deficie
79  one of the two primary carcinogenic routes: chemical carcinogenesis through exposure to tobacco and
80 study, we used an established mouse model of chemical carcinogenesis to investigate how 1,25-VD preve
81       Thus, tissue-associated DC can enhance chemical carcinogenesis via PAH metabolism, highlighting