chrysarobin/carcinogenesis

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Skin carcinogenesis: characteristics, mechanisms, and prevention.

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Identifikohuni Regjistrohu

Skin carcinogenesis can be operationally and mechanistically divided into at least three major stages - initiation, promotion and progression. Variations among stocks and strains of mice to susceptibility to multistage skin carcinogenesis appear to be more related to alterations in tumor promotion

Skin tumorigenesis by initiators and promoters of different chemical structures in lines of mice selectively bred for resistance (Car-r) or susceptibility (Car-s) to two-stage skin carcinogenesis.

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Identifikohuni Regjistrohu

Carcinogenesis-resistant (Car-R) and carcinogenesis-susceptible (Car-S) mice were obtained applying a bi-directional selective breeding approach to a two-stage skin carcinogenesis protocol, using 9,10-dimethyl-1,2-benzanthracene (DMBA) as initiator and 12-O-tetradecanoylphorbol-13-acetate (TPA) as

Dose-response relationship in multistage carcinogenesis: promoters.

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Identifikohuni Regjistrohu

Published dose-response curves of promoters of multistage carcinogenesis were selected that met the combined criteria of long study times, multiple doses, and low doses. In rat liver, 12 dose-response studies of 7 different promoters (phenobarbital, 2,3,7,8-tetrachlorodibenzo-p-dioxin [TCDD],

Induction or suppression of SV40 amplification by genotoxic carcinogens, non-genotoxic carcinogens or tumor promoters.

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Identifikohuni Regjistrohu

Carcinogens are generally classified into two groups: genotoxic and non-genotoxic. As the final product of genotoxic and non-genotoxic carcinogens is the same, i.e., a clone of genetically altered cells, it could be possible that non-genotoxic carcinogens may yield genotoxic events as a secondary

Epidermal growth factor receptor-mediated activation of Stat3 during multistage skin carcinogenesis.

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Identifikohuni Regjistrohu

In the present study, we have investigated the possible role of signal transducers and activators of transcription (STATs), particularly Stat3, in mouse skin tumor promotion and multistage carcinogenesis. Stat1, Stat3, and Stat5 were activated in mouse epidermis after treatment with different

Further studies on the influence of initiation dose on papilloma growth and progression during two-stage carcinogenesis in SENCAR mice.

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Identifikohuni Regjistrohu

The present study was designed to further evaluate the growth and progression of papillomas to squamous cell carcinomas (SCCs) in groups of animals receiving initiating doses of 7,12-dimethylbenz[a]anthracene (DMBA) producing relatively low papilloma yields following long term promotion (60 weeks)

Malignant conversion, the first stage in progression, is distinct from phorbol ester promotion in mouse skin.

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Identifikohuni Regjistrohu

Papillomas induced by DMBA initiation-TPA promotion protocols are necessary precursor lesions of squamous cell carcinomas. The papillomas are heterogeneous in their potential for progression to carcinomas, a property apparently induced at the time of initiation. The probability of conversion to

Effect of diverse tumor promoters on the expression of gap-junctional proteins connexin (Cx)26, Cx31.1, and Cx43 in SENCAR mouse epidermis.

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Identifikohuni Regjistrohu

The inhibition of gap-junctional intercellular communication (GJIC) between initiated and surrounding normal cells by tumor promoters is believed to be important in the promotion stage of carcinogenesis. Therefore, we examined the effect of skin-tumor promoters on the expression of the

Proteomic and pathway analyses reveal a network of inflammatory genes associated with differences in skin tumor promotion susceptibility in DBA/2 and C57BL/6 mice.

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Identifikohuni Regjistrohu

Genetic susceptibility to two-stage skin carcinogenesis is known to vary significantly among different stocks and strains of mice. In an effort to identify specific protein changes or altered signaling pathways associated with skin tumor promotion susceptibility, a proteomic approach was used to

Inhibition of the glucocorticoid receptor expression by diverse tumor promoters in SENCAR mouse epidermis.

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Identifikohuni Regjistrohu

Glucocorticoid hormones are very potent inhibitors of keratinocyte proliferation. Their function is mediated by the glucocorticoid receptor (GR) which is highly expressed in mouse epidermis. In the study reported here we compared the effect of 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and

Activation of the epidermal growth factor receptor by skin tumor promoters and in skin tumors from SENCAR mice.

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Identifikohuni Regjistrohu

The present study was designed to further investigate the role of the epidermal growth factor receptor (EGFr) in mouse skin tumor promotion by evaluating the status of the EGFr in tumor promoter-treated mouse epidermis and in mouse skin tumors. Female SENCAR mice received three topical treatments of

A novel mechanism of skin tumor promotion involving interferon-gamma (IFNγ)/signal transducer and activator of transcription-1 (Stat1) signaling.

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Identifikohuni Regjistrohu

The current study was designed to explore the role of signal transducer and activator of transcription 1 (Stat1) during tumor promotion using the mouse skin multistage carcinogenesis model. Topical treatment with both 12-O-tetradecanoylphorbol-13-acetate (TPA) and 3-methyl-1,8-dihydroxy-9-anthrone

Altered expression of epidermal growth factor receptor ligands in tumor promoter-treated mouse epidermis and in primary mouse skin tumors induced by an initiation-promotion protocol.

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Identifikohuni Regjistrohu

Multiple epidermal growth factor receptor (EGFr) ligands have been identified, including transforming growth factor alpha (TGFalpha), heparin-binding epidermal growth factor (HB-EGF), amphiregulin (AR), and betacellulin (BTC). Previous work from our laboratory demonstrated that TGFalpha mRNA and

Tumor progression in Sencar mouse skin as a function of initiator dose and promoter dose, duration, and type.

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Identifikohuni Regjistrohu

The influence of initiator dose and promoter dose, duration, and type on the progression of papillomas to carcinomas was examined in Sencar mice. A good dose-response relationship for promotion of papilloma formation by 12-O-tetradecanoylphorbol-13-acetate (TPA) [following initiation with 6.5

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