No abstract available.
9,10-Dimethyl-1,2-benzanthracene* ; Tocopherols*

No abstract available.
9,10-Dimethyl-1,2-benzanthracene* ; Animals ; Breast Neoplasms* ; Breast* ; Estrogens* ; Rats*

No abstract available.
9,10-Dimethyl-1,2-benzanthracene* ; Carcinogenesis* ; Hyperbaric Oxygenation* ; Submandibular Gland*

No abstract available.
9,10-Dimethyl-1,2-benzanthracene ; Animals ; Rats ; Submandibular Gland

PURPOSE: This study was carried out to investigate the effect of irradiation on the expression of proliferating cell nuclear antigen (PCNA) and apoptosis induction during the carcinogenesis in hamster buccal pouch. MATERIALS AND METHODS: Three months old Syrian golden hamsters were divided into control and 2 experimental groups. Hamsters in control group were left untreated on buccal pouchs. Twenty four hamsters were treated with 0.5% DMBA tri-weekly on the right buccal pouch. Forty eight hamsters were treated with 0.5% DMBA tri-weekly and irradiated with the dose of 5 Gy and 10 Gy at 6, 9, 12, 15 weeks after DMBA application. Resected buccal pouches were sectioned and examined for potential expression pattern of PCNA and apoptosis. RESULTS: The PCNA index was increased with the stages of buccal pouch epithelium carcinogenesis except the hyperplasia stage in control group (p<0.05). The irradiation did not effect on the PCNA index in the dysplasia and the carcinoma in situ stage, but in the hyperplasia stage, the PCNA index was increased with 10 Gy radiation and decreased in the carcinoma stage (p<0.05). The apoptotic index was significantly decreased from the carcinoma in situ stage and the lowest in the carcinoma stage. The apoptotic index was significantly decreased in the hyperplasia and dysplasia stage with the 5 Gy irradiation and significantly increased only in the carcinoma stage with the 10 Gy irradiation (p<0.05). CONCLUSION: The PCNA and apoptotic index were varied according to the irradiation period and dosage in each carcinogenesis stage.
9,10-Dimethyl-1,2-benzanthracene* ; Animals ; Apoptosis* ; Carcinogenesis* ; Carcinoma in Situ ; Cricetinae* ; Epithelium ; Hyperplasia ; Mesocricetus ; Proliferating Cell Nuclear Antigen* ; Radiation Dosage

PURPOSE: To understand the morphologic and molecular changes in carcinogen-induced breast tissues, DMBA (10-dimethy1-1,2 benzanthracene) was administrated in Sprague- Dawley female rats. MATERIALS AND METHODS: At 50 days of age, all experimental rats were given 20 mg DMBA by gastric intubation. Until the seventh week after DMBA administration, six rats were sacrificed every week, thereafter all tumors found during 20 weeks were removed every week. The morphologic changes were evaluated in routinely processed sections stained with H-E and with anti-smooth muscle actin antibody. Mutation of Ha-ras codons 12 and 61 was examined by ARMS (amplification refractory mutation system) method in frozen tissues. RESULTS: The epithelial cell proliferation of terminal end buds began 2 weeks after DMBA treatment and progressed to the 6th week, resulting in microscopic malignant tumor in one of the 7th weeks rats. The tumors were developed in 43 of 62 rats (69.4%); 8 benign lesions in 4 rats and 72 malignant tumors in 39 rats. Mutations in the 12th and 61th codon of Ha-ras gene were respectively found in 29.7% and 2.7% of preneoplastic breasts, 25% in benign lesions, 2.6% and 31.6% of malignant tumors. CONCLUSION: DMBA treatment in rats induced epithelial proliferation, then benign and malignant tumors through Ha-ras gene mutation, especially in codon 61 leading to cancer.
9,10-Dimethyl-1,2-benzanthracene* ; Actins ; Animals ; Arm ; Breast ; Codon ; Epithelial Cells ; Female ; Genes, ras ; Humans ; Intubation ; Rats*

Cellular transforming genes have been identified in a number of different tumor cell lines and tumor types. A significant number of these oncogenes belong to the ras gene family. The ras gene family consists of three closely related genes:H-ras, K-ras and N-ras which code for a related 21 kDa protein. Mutations in codon 12, 13 and 61 of one of the three ras genes convert these genes into acute oncogenes. The presence of H-ras gene mutaions has important prognostic implication in various tumors. Each genomic DNA was isolated from tumors induced by implantation with DMBA, or by treatment with DMBA-implantation/irradiation. When genome DNA was transfected into NIH 3T3 cells and investigated by two-step PCR-RFLP, the following results were concluded : 1. Transformation foci developed in two groups when the genome DNA of two experimental groups were transfected into NIH 3T3 cells. 2. Transformation efficiency was 0.01-0.02 foci/ DNA in the experimental group with the DMBA-implantation, 0.01-0.03 foci/ DNA in the experimental group with the DMBA-implantation/irradiation according to results of trasfection assay. 3. When the point mutation of H-ras gene was investigated by a two-step PCR-RFLP, there was 13.9%(5/36) in the experimental group with the DMBA implantation, 15.4%(6/39) in the experimental group with the DMBA-implantation/irradiation. 4. The point mutation in codon 12 and 61 of H-ras was 5.6%(2/36) and 8.3%(3/36) in the experimental group with the DMBA implantation. 5. The point mutation in codon 12 and 61 of H-ras gene was 7.7%(3/39) in the experimental group with the DMBA-implantation/irradiation.
9,10-Dimethyl-1,2-benzanthracene* ; Animals ; Cell Line, Tumor ; Codon ; DNA ; Genes, ras* ; Genome ; Humans ; NIH 3T3 Cells ; Oncogenes ; Point Mutation ; Rats* ; Salivary Glands*

PURPOSE: The incidence of salivary gland tumor is approximately 2% among all head and neck tumors, of which malignant cases account for only about 5%. Much research has been performed in order to clarify the mechanism of oncogene activation, however salivary gland tumors remain understudied. We performed this study in order to characterize the ras gene in these tumors. MATERIALS AND METHODS: We treated white rats with 7, 12-dimethylbenz[a]anthracene (DMBA) and confirmed the occurrence of salivary gland tumors after ten to thirty weeks. Isolated genomic DNAs from tumor tissues were added to NIH 3T3 cells. In order to detect Ha-ras mutations, we performed a two-step PCR-RFLP and 7analyzed the mutated sequences. RESULTS: We induced salivary gland tumors by DMBA treatment in white rats. Isolated DNAs from the tumor tissues transformed the NIH 3T3 cells. Point mutations were observed in codons 12 and 61 of the Ha-ras oncogene. The total frequency of point mutations was 13.9% in DMBA-induced salivary gland tumors in rats. CONCLUSION: Our results demonstrate that a variety of cancers ras oncogene mutations were also found in salivary gland tumors. We confirmed that a point mutation of the Ha-ras oncogene in a DMBA-induced salivary gland tumor occurs at a frequency of 13.9%.
9,10-Dimethyl-1,2-benzanthracene* ; Animals ; Codon ; DNA ; Genes, ras* ; Head ; Incidence ; Neck ; NIH 3T3 Cells ; Oncogenes ; Point Mutation ; Rats* ; Salivary Glands*

BACKGROUND: It has been suggested that mast cells are involved in the tumor growth and progression by production of a variety of enzymes and growth factors. They were studied in the 10-dimethyl-1,2 benzanthracene (DMBA)-induced rat mammary tumors, and evaluated in relation with the production of tryptase, chymase, and matrix metalloproteinase (MMP)-2 and MMP-9. METHODS: Preneoplastic and neoplastic breast tissues of Sprague-Dawley female rats were obtained every week after DMBA treatment for 12 weeks. Toluidine blue stain was used for the identification of mast cells. Mast cell tryptase was studied by immunohistochemistry, and chymase by esterase stain. MMP-2 and MMP-9 were measured by Western blotting. RESULTS: The numbers of mast cells in breast cancers were higher than in preneoplastic tissues, and there was a positive correlation between the numbers of tryptase-positive cells and the tumor size. MMP-9 quantity was correlated with the numbers of toluidine blue and chymase positive cells, but not with tryptase-positive cells and tumor size. Both active and inactive forms of MMP-2 and MMP-9 were identified in zymogram. CONCLUSIONS: The mast cells are increased in the DMBA-induced breast cancers, and their tryptase and chymase may play a role in tumor progression with or without participation of MMP-2 and MMP-9.
9,10-Dimethyl-1,2-benzanthracene ; Animals ; Blotting, Western ; Breast ; Chymases ; Female ; Humans ; Immunohistochemistry ; Intercellular Signaling Peptides and Proteins ; Mast Cells* ; Rats* ; Rats, Sprague-Dawley ; Tolonium Chloride ; Tryptases

OBJECTIVES: The aim of this study was to verify the promoting effect of carbamide peroxide on dimethylbenzanthracene (DMBA)-induced carcinogenesis in the hamster buccal pouch, in order to reduce the period of latency for tumor formation. METHODS: Sixteen hamsters were randomized into two groups of eight animals each. The hamsters of the group I had their right buccal pouches treated with 0.5% DMBA and 10% carbamide peroxide teeth bleaching gel for 55 days. The animals of the group II had their right pouches treated only with DMBA. After, six animals of each group had their pouches prepared for light microscopy. Histomorphometry was performed to assess the presence of keratinization, nuclear polymorphism, pattern of invasion, number of blood vessels, and inflammatory infiltrate in the tumor front. Furthermore, the newly formed lesions were graded according the Bryne's grading system. The remaining animals had the vascular system of the pouches casted by Mercox and qualitatively analyzed by scanning electron microscopy. RESULTS: Histopathological analysis of the buccal pouches treated with DMBA and carbamide peroxide exhibited formation of squamous cell carcinoma well-differentiated with a high degree of malignancy in all pouches. The development of this neoplasm was associated with a significant increase in the number of blood vessels, presence of keratin pearls, and inflammatory infiltrate. The pouches of the group II showed inflammation, epithelial hyperplasia, dysplasia, and squamous cell carcinoma in only three right pouches. The analysis of the electron micrographs of the pouches chemically inducted with DBMA and carbamide peroxide reveled formation of a new vascular network characteristic of squamous cell carcinoma. CONCLUSION: The protocol presented here, using DMBA associated with carbamide peroxide, shortens the period of latency to produce squamous cell carcinoma in the hamster buccal pouch, decreasing the time and costs of the experiments.
9,10-Dimethyl-1,2-benzanthracene ; Animals ; Blood Vessels ; Carcinogenesis ; Carcinogens ; Carcinoma, Squamous Cell ; Cricetinae* ; Head and Neck Neoplasms* ; Hyperplasia ; Inflammation ; Microscopy ; Microscopy, Electron, Scanning ; Tooth Bleaching* ; Urea*