Carcinogen-induced granulosa cell tumours in NZC/BL MICE

Geary, C. P. M.

doi:10.3109/00313028409059090

Cited by 7 publications

(3 citation statements)

References 15 publications

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“…The poly-cyclic aromatic hydrocarbon and known carcinogen, 7,12-dimethylbenzanthracene (DMBA) was chosen to induce the cancerous phenotype, because it is well-characterized and has been shown to increase the incidence endometrial hyperplasia and uterine polyps in mice (Geary, 1984; Gray et al 1997). Karyometric analysis and the soft-agar colony forming assay were used to confirm the development and prevention of the cancerous phenotype in the organotypic cultures (Ranger-Moore et al 2005).…”

Section: Introductionmentioning

confidence: 99%

“…The objective of this study was to develop and characterize an organotypic model of endometrial carcinogenesis and Flex-Het chemprevention and to identify molecules in this model that are regulated in opposite directions during the processes of carcinogenesis and chemoprevention. The polycyclic aromatic hydrocarbon and known carcinogen, 7,12-dimethylbenzanthracene (DMBA) was chosen to induce the cancerous phenotype, because it is well-characterized and has been shown to increase the incidence endometrial hyperplasia and uterine polyps in mice (Geary, 1984;Gray et al 1997). Karyometric analysis and the soft-agar colony forming assay were used to confi rm the development and prevention of the cancerous phenotype in the organotypic cultures (Ranger- Moore et al 2005).…”

Section: Introductionmentioning

confidence: 99%

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Gene Expression Analysis of Biological Systems Driving an Organotypic Model of Endometrial Carcinogenesis and Chemoprevention

Benbrook

Lightfoot

Ranger‐Moore

et al. 2008

Gene�Regul Syst Bio

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An organotypic model of endometrial carcinogenesis and chemoprevention was developed in which normal endometrial organotypic cultures exposed to the carcinogen, DMBA (7,12-dimethylbenz[a]anthracene), developed a cancerous phenotype in the absence, but not presence of subsequent treatment with a flexible heteroarotinoid (Flex-Het), called SHetA2. A discriminant function based on karyometric features of cellular nuclei and an agar clonogenic assay confirmed these histologic changes. Interpretation of microarray data using an internal standard approach identified major pathways associated with carcinogenesis and chemoprevention governed by c-myc, p53, TNFα and Jun genes. Cluster analysis of functional associations of hypervariable genes demonstrated that carcinogenesis is accompanied by a stimulating association between a module of genes that includes tumor necrosis factor α (TNFα), c-myc, and epidermal growth factor-receptor (EGF-R) and a module that includes insulin-like growth factor I-receptor (IGF-IR), p53, and Jun genes. Two secreted proteins involved in these systems, tenascin C and inhibin A, were validated at the protein level. Tenascin C is an EGF-R ligand, and therefore may contribute to the increased EGF-R involvement in carcinogenesis. The known roles of the identified molecular systems in DMBA and endometrial carcinogenesis and chemoprevention supports the validity of this model and the potential clinical utility of SHetA2 in chemoprevention.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Gene Expression Analysis of Biological Systems Driving an Organotypic Model of Endometrial Carcinogenesis and Chemoprevention

Benbrook

Lightfoot

Ranger‐Moore

et al. 2008

Gene�Regul Syst Bio

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“…Breeder females showed a zero incidence for the same time frame. Telangiectasis principally affecting vessels in the ovary, uterus, and small intestine (83.3%) was a common finding in NZC/BL mice treated with 7,12-dimethylbenz[a]anthracene (31).…”

Section: Vascular Lesionsmentioning

confidence: 99%

Nonneoplastic lesions of the ovary in Fischer 344 rats and B6C3F1 mice.

Montgomery

Alison

1987

Environ Health Perspect

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The National Toxicology Program's pathology database on 2-year carcinogenicity studies was reviewed for nonneoplastic ovarian disease. Ovaries from 39,941 female Fischer rats and 41,444 female B6C3F1 mice were examined. A variety of inflammatory, degenerative, vascular, and proliferative lesions were documented and are described. The most common ovarian lesions in rats were cysts (6%). The most frequent ovarian lesions in mice were cysts (15%), acute inflammation (4%), degeneration (4%), vascular disease (2.5%), and atrophy (2%). There was no difference in incidence of ovarian disease between controls and treated animals. The frequency of ovarian disease in mice exceeded the frequency in rats in every category.

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Animal Models for Tumors of the Female Genital Tract

Marchant¹

1987

Blaustein’s Pathology of the Female Genital Tract

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Carcinogen-induced granulosa cell tumours in NZC/BL MICE

Cited by 7 publications

References 15 publications

Gene Expression Analysis of Biological Systems Driving an Organotypic Model of Endometrial Carcinogenesis and Chemoprevention

Gene Expression Analysis of Biological Systems Driving an Organotypic Model of Endometrial Carcinogenesis and Chemoprevention

Nonneoplastic lesions of the ovary in Fischer 344 rats and B6C3F1 mice.

Animal Models for Tumors of the Female Genital Tract

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