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*

This experiment was performed to elucidate the cytologic origin of chemically induced MFH in Wistar rats. The tumor was produced by injections of DMBA(9,10-dimethyl-1,2-benzanthracene). With the produced MFH, cell culture and cloning were performed, followed by establishment of a cell strain, which was investigated by immunohistochemical and electron microscopic studies. The results were as follows. A) By immunohistochemistry of the tumor tissue, fibroblastic cells were positive for MEP-1(specific antibody for fibroblastlike cell of MFH, Takeya, 1993) and Anti-hPH(beta)(Anti-prolyl 4-hydroxylase beta), but negative for TRPM-3 and F4/80. Histiocytelike cells were positive for TRPM-3 and F4/80, but negative for MEP-1 and Anti-hPH(beta). In immunoelectron microscopy, normal spleen macrophage showed linear reactivity in cell membrane for TRPM-3, whereas histiocytelike cells of the tumor disclosed negative reaction. B) At 5 weeks of the primary tumor cell culture, the cells exhibited typical storiform pattern of MFH. C) The established cell strain revealed immunoreactivity for MEP-1 and Anti-hPH(beta), but negative for TRPM-3. The cloned tumor cells showed morphologic characteristics of undifferentiated fibroblastic cell. Latex particle (0.80 micrometer size) phagocytosis was negative in the cloned cell strain. The results of the current study support the concept that principal component cells of MFH is of fibroblastic cell origin.
9,10-Dimethyl-1,2-benzanthracene* ; Animals ; Cell Culture Techniques* ; Cell Membrane ; Clone Cells* ; Cloning, Organism* ; Fibroblasts ; Histiocytoma, Malignant Fibrous* ; Immunohistochemistry ; Macrophages ; Microscopy, Immunoelectron ; Microspheres ; Phagocytosis ; Rats* ; Rats, Wistar ; Spleen

Angiogenesis inhibition is major concern to cancer chemotherapy and many studies about compound inhibiting angiogenesis is in progression. The long-known preventive effect of plant-based diet on tumorigenesis and other chronic diseases is well documented. Especially soy extract, genistein, is known to be potent angiogenesis inhibitor and prevent development and progression of tumor. In the present study, the effect of angiogenesis on tumorigenesis and chemopreventive effect of genistein by angiogenesis inhibition in hamster buccal pouch oral carcinigenesis model induced by 7.12-dimethylbenza(a)nthracene (DMBA) was studied. Forty eight Syrian Golden young adult hamsters (150-200 gm) were divided into two groups. In control group, 0.5% DMBA in heavy mineral oil was applied to hamster buccal pouch three times a week and in experimental group, 0.1 mg of genistein is administered orally everyday in addition to DMBA application. The animals were euthanized from 2 weeks to 16 weeks with interval of 2 week. HandE staining and immunohistochemistry was performed to evaluate microvessel density by using factor VIII-related antigen and avidin-biotin technique. Microvessels per area was quantified and compared between control and experimental group statistically. The results were as follows. 1. Microvessel density was increased time dependently in both groups and especially the increase was significant from 12 weeks to 16 weeks. 2. When comparing both group, the experimental group showed significantly low microvessel density than control group in 12 weeks (p=0.043), 14 weeks (p=0.050), 16 weeks (p=0.037). Based on these results, it was concluded that genistein influenced oral carcinogenesis by angiogenesis inhibition.
9,10-Dimethyl-1,2-benzanthracene ; Animals ; Carcinogenesis* ; Chronic Disease ; Cricetinae ; Diet ; Drug Therapy ; Genistein* ; Hand ; Humans ; Immunohistochemistry ; Microvessels ; Mineral Oil ; von Willebrand Factor ; Young Adult

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*

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*