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: 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*

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

BACKGROUND: In order to investigate the roles of p16 and Rb, their expression was evaluated in 9,10-dimethyl-1,2-benzanthracene (DMBA)-induced ovarian cancers of rats. METHODS: DMBA-coated silk was inserted into both ovaries of 20 9-week-old Sprague-Dawley rats. The experimental period lasted 20 weeks. The tumor histology was classified and the expression of p16 and Rb in the ovarian tumors was analyzed by immunohistochemistry and Western blot. RESULTS: The p16 and Rb labeling index was significantly lower in the ovarian cancers than the normal ovarian surface epithelium of a rat. There were no differences among the cancer types. In Western blot analysis, the expressions of p16 and Rb in ovarian cancers were lower than those in normal ovarian tissue. No correlation was present between p16 and Rb. CONCLUSION: The abnormal expression of p16 and Rb occurs in DMBA-induced rat ovarian cancer and might be involved in carcinogenesis.
9,10-Dimethyl-1,2-benzanthracene* ; Animals ; Blotting, Western ; Carcinogenesis* ; Epithelium ; Female ; Immunohistochemistry ; Ovarian Neoplasms ; Ovary ; Rats* ; Rats, Sprague-Dawley ; Retinoblastoma Protein ; Silk

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

OBJECTIVETo study the immunotoxicity induced by 9,10-dimethyl-1,2-benzathrancene (DMBA) in metallothionein gene-knocked-out mice [MT(-/-)] as compared with that in wild-type mice [(MT(+/+)].

METHODSFemale mice were treated with 25 mg/kg and 50 mg/kg of DMBA i.p., respectively and immunized with sheep red blood cells (SRBC) i.v. on the following day and rechallenged by injection of SRBC via footpad s.c. on the fourth day post-immunization. Humoral and cell-mediated immune function was assessed by the number of spleen IgM antibody plaque formation cells (PFC) to SRBC and cell-mediated delayed-type hypersensitivity (DTH) measured by footpad swelling thickness.

RESULTSAfter treatment with 25 mg/kg DMBA, a decrease in weight of their spleen and thymus and PFC/spleen were observed in MT(-/-) mice, while only decrease in thymus weight of MT(+/+) mice. The humoral function was suppressed by 72% in MT(-/-) mice. No obvious change in cell-mediated immune function was observed both in MT(-/-) and MT(+/+) mice. Both humoral and cell-mediated immune function were suppressed more severe (91%) in MT(-/-) mice treated with 50 mg/kg DMBA than those treated with 25 mg/kg DMBA (72%). DTH was not altered by DMBA in MT(+/+) mice. The weight of their spleen and thymus decreased and humoral immune function suppressed in MT(+/+) mice, but these changes were significantly less severe. No obvious suppression of cell-mediated immune function was observed in MT(+/+) mice.

CONCLUSIONTheir humoral and cell-mediated immune function was more susceptible to being suppressed by DMBA in MT(-/-) mice, indicating that MT could protect their immune function from damage caused by DMBA.

9,10-Dimethyl-1,2-benzanthracene ; toxicity ; Animals ; Immunity ; drug effects ; Metallothionein ; physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Organ Size ; drug effects