Disease relevance of Mice, Inbred SENCAR

• In this study, we assessed the protective effect of topical application of a polyphenolic fraction isolated from green tea (GTP) against spontaneous as well as benzoyl peroxide (BPO)- and 4-nitroquinoline-N-oxide (4-NQO)-enhanced malignant conversion of chemically induced skin papillomas in SENCAR mice [1].
• The antiinflammatory steroid fluocinolone acetonide, an inhibitor of TPA-induced hyperplasia, as well as the multiple stages of tumor promotion as defined in SENCAR mice (Stages I and II), inhibited the TPA-dependent elevation of epidermal XO activity [2].
• At higher doses (1-10 mumol), CAPE inhibits edema and ornithine decarboxylase induction in CD-1 and SENCAR mice [3].
• To test the hypothesis that acrylamide should possess carcinogenic properties, it was tested in the Salmonella-microsome assay for point mutation, as a skin tumor initiator in the Sencar mouse, and for its ability to induce lung adenomas in the A/J mouse [4].
• Ovariectomy increases squamous metaplasia of the uterine horns and survival of SENCAR mice fed a vitamin A-deficient diet [5].

Psychiatry related information on Mice, Inbred SENCAR

• To histologically define the effect of low dietary calcium on bone metabolism, we performed histomorphometric analysis of tetracycline-labeled sections of femoral bone from male SENCAR mice maintained on calcium-sufficient and calcium-deficient diets during the critical period from 10 to 14 weeks of age [6].

High impact information on Mice, Inbred SENCAR

• Furthermore, in the NMRI mouse, PRA is a much more potent second-stage promoter than mezerein, recently reported to be an incomplete promoter in the Sencar mouse [7].
• The effects of fluocinolone acetonide (FA), retinoic acid (RA), and tosylphenylalanine chloromethyl ketone (TPCK) on two-stage promotion after 7,12-dimethylbenz[a]-anthracene (DMBA) initiation in female Sencar mice were investigated [8].
• A flavonoid antioxidant, silymarin, affords exceptionally high protection against tumor promotion in the SENCAR mouse skin tumorigenesis model [9].
• Preapplication of GE onto the skin of SENCAR mice resulted in significant inhibition of 12-0-tetradecanoylphorbol-13-acetate (TPA)-caused induction of epidermal ODC, cyclooxygenase, and lipoxygenase activities and ODC mRNA expression in a does-dependent manner [10].
• Transplacental carcinogenicity of cisplatin: initiation of skin tumors and induction of other preneoplastic and neoplastic lesions in SENCAR mice [11].

Chemical compound and disease context of Mice, Inbred SENCAR

• Papillomas were induced in 7,12-dimethylbenz[a]anthracene (DMBA)-initiated SENCAR mouse epidermis by (i) complete promotion with benzoyl peroxide; (ii) complete promotion with 12-O-tetradecanoyl phorbol-13-acetate (TPA); and (iii) two-stage promotion with TPA for 2 weeks followed by mezerein for 9 weeks [12].
• Regression and progression characteristics of papillomas induced by chrysarobin in SENCAR mice [13].
• Differential effects of dietary beta-carotene on papilloma and carcinoma formation induced by an initiation-promotion protocol in SENCAR mouse skin [14].
• Application of the alkane n-dodecane to the dorsal skin of 6-8 week old female SENCAR mice initiated with 10 nmol dimethylbenz[a]anthracene led to papilloma formation in the majority of treated animals [15].
• Since the proliferative agent ethylphenylpropiolate had no effect on protein kinase C in epidermis from SENCAR mice, the ability of benzoyl peroxide to influence protein kinase C activity in mouse skin may reflect its tumor promoting capabilities rather than its ability to induce hyperplasia [16].

Biological context of Mice, Inbred SENCAR

• Here, we made a sequential study of alterations in cell cycle protein expression and complex formation among cyclin, cyclin dependent kinases (CDKs) and CDK inhibitors (CKIs) during premalignant progression in SENCAR mouse skin tumors [17].
• Intraperitoneal injection of 50 micrograms/g pentoxifylline at 30 min prior to topical application of 10 micrograms TPA to the dorsal epidermis of Sencar mice inhibited TPA-induced IL-1 alpha and TNF-alpha gene expression 24 h after TPA treatment [18].
• The skin and lung tissues from SENCAR mice used as part of the Environmental Protection Agency's (EPA's) Carcinogenesis Testing Matrix were examined [19].
• Serum osteocalcin (an index of bone formation) was higher in C57BL/6 mice than in SENCAR mice [20].
• OBJECTIVE: In the present work we studied the association of histamine receptors with second messengers during multistage carcinogenesis in Sencar mice skin [21].

Anatomical context of Mice, Inbred SENCAR

• Enhanced release of hydrogen peroxide and metabolites of arachidonic acid by macrophages from SENCAR mice following stimulation with phorbol esters [22].
• The induction and fate of pyrimidine dimers and unscheduled DNA synthesis were measured in u.v.-irradiated primary, newborn SENCAR mouse epithelial cells [23].
• Recent studies from this laboratory have shown that TPA significantly enhances formation of hydrogen peroxide (H2O2) and oxidized DNA bases in SENCAR mouse skin, as it increases the infiltration of polymorphonuclear leukocytes (PMNs), as quantitated by myeloperoxidase (MPO) [24].
• Cell line SCR722 was derived from adult SENCAR mouse epidermal cells initiated in culture by treatment with the carcinogen N-methyl-N'-nitro-N-nitrosoguanidine and selection for foci proliferating in medium with calcium levels that induce terminal differentiation in normal cells [25].
• Cultures of keratinocytes obtained from dorsal skins of female SENCAR mice were exposed to 0.5 microgram of tritium-labeled hydrocarbons/mL of medium for 24 h [26].

Associations of Mice, Inbred SENCAR with chemical compounds

• Alterations in epidermal polyamine levels and DNA synthesis following topical treatment with chrysarobin in SENCAR mice [27].
• In a number of independent experiments, either with female CD-1 or SENCAR mice, we failed to observe a specificity of inhibition by retinoic acid of either Stage I or Stage II tumor promotion [28].
• The skin tumor-promoting ability of 1,8-dihydroxy-3-methyl-9-anthrone (chrysarobin) was compared with that of 12-O-tetradecanoylphorbol-13-acetate (TPA) and 1,8-dihydroxy-9-anthrone (anthralin) in SENCAR mice [29].
• Female SENCAR mice initiated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were promoted twice weekly with 12-O-tetradecanoylphorbol-13-acetate (TPA) [30].
• Effect of dietary tannic acid on epidermal, lung, and forestomach polycyclic aromatic hydrocarbon metabolism and tumorigenicity in Sencar mice [31].

Gene context of Mice, Inbred SENCAR

• Ornithine decarboxylase expression in cutaneous papillomas in SENCAR mice is associated with altered expression of keratins 1 and 10 [32].
• Comparison of histologic changes in skin revealed that wa-1 mice exhibited only modest sustained epidermal hyperplasia after multiple treatments with TPA, similar in magnitude to that of C57BL/6 mice and significantly lower than that of SENCAR mice [33].
• Dietary energy restriction inhibits ERK but not JNK or p38 activity in the epidermis of SENCAR mice [34].
• Significant inhibition by the flavonoid antioxidant silymarin against 12-O-tetradecanoylphorbol 13-acetate-caused modulation of antioxidant and inflammatory enzymes, and cyclooxygenase 2 and interleukin-1alpha expression in SENCAR mouse epidermis: implications in the prevention of stage I tumor promotion [35].
• In the present study, we used monospecific keratin antibodies to show the expression and distribution of keratins in SENCAR mouse vaginal epithelium in different stages of the estral cycle and in ovariectomized animals [36].

Analytical, diagnostic and therapeutic context of Mice, Inbred SENCAR

• We have examined these Calcium (Ca)-resistant cells formed in the skin of SENCAR mice after treatment with the carcinogen initiator 7,12-dimethylbenz[a]anthracene (DMBA) followed by tumor promotion with 12-O-tetradecanoylphorbol-13-acetate (TPA) [37].
• Oral administration of the citrus coumarin, isopimpinellin, blocks DNA adduct formation and skin tumor initiation by 7,12-dimethylbenz[a]anthracene in SENCAR mice [38].
• Northern blot analysis indicated that topical application of TPA, anthralin, mezerein, or benzoyl peroxide to SENCAR mice resulted in an increased expression of epidermal IL-1 alpha mRNA [39].
• Membrane proteins from SENCAR mouse epidermis were isolated 6 h after the last treatment, and the phosphotyrosine content of the EGFr and several potential substrates were examined by Western blot analysis [40].
• Using quercetin as the internal standard, a reversed-phase HPLC method was developed to quantitatively analyze apigenin in epidermal cells obtained from SENCAR mice [41].

References