Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of murine mammary glands to study early events occuring in p53-independent hormone-induced tumorigenesis

ABSTRACT: LH-overexpressing mice display elevated levels of mammogenic hormones and consequently develop spontaneous mammary tumors with a median latency of 41 weeks. Tumors occur in the absence of p53 mutations and in the presence of a seemingly functional p53 signaling pathway. At 16 weeks of age, no histological evidence of tumors is observed in these transgenic mammary glands; however, mammary cells do demonstrate centrosome amplification at this age suggesting that early tumorigenic processes may have occured. Thus comparison of the transcriptome of the mammary glands from 16 week old LH-overexpressing mice to that of wild type mice will provide insight into early events occuring in p53-independent hormone-induced tumorigenesis. Experiment Overall Design: Total RNA was isolated from mammary glands of a total of 9 wild type and 9 transgenic mice. RNA from 3 mammary glands was pooled together generating 3 wild type samples and 3 transgenic samples.

ORGANISM(S): Mus musculus

SUBMITTER: Ruth Keri

PROVIDER: E-GEOD-3348 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:The present experiments were performed to determine the roles of estrogen receptors M-NM-1 and M-NM-2 (ERM-NM-1 and ERM-NM-2) in normal and neoplastic development in the mouse mammary gland. In wild-type mice, in vivo administration of estradiol (E) + progesterone (P) stimulated mammary ductal growth and alveolar differentiation. Mammary glands from mice in which the ERM-NM-2 gene has been deleted (M-NM-2ERKO mice) demonstrated normal ductal growth and differentiation in response to E + P. By contrast, mammary glands from mice in which the ERM-NM-1 gene has been deleted (M-NM-1ERKO mice) demonstrated only rudimentary ductal structures that did not differentiate in response to E + P. EGF demonstrates estrogen-like activity in the mammary glands of M-NM-1ERKO mice: treatment of M-NM-1ERKO mice with EGF + P (without E) supported normal mammary gland development, induced expression of progesterone receptor (PR), and increased levels of G- protein-coupled receptor (GPR30) protein. Mammary gland development in M-NM-2ERKO mice treated with EGF + P was comparable to that of wild-type mice receiving EGF + P; EGF had no statistically significant effects on the induction of PR or expression of GPR30 in mammary glands harvested from either wild-type mice or M-NM-2ERKO mice. In vitro exposure of mammary glands to 7,12-dimethylbenz[a]anthracene (DMBA) induced preneoplastic mammary alveolar lesions (MAL) in glands from wild-type mice and M-NM-2ERKO mice, but failed to induce MAL in mammary glands from M-NM-1ERKO mice. Microarray analysis of DMBA-treated mammary glands identified 28 functional pathways whose expression was significantly different in M-NM-1ERKO mice versus both M-NM-2ERKO and wild-type mice; key functions that were differentially expressed in M-NM-1ERKO mice included cell division, cell proliferation, and apoptosis. The data demonstrate distinct roles for ERM-NM-1 and ERM-NM-2 in normal and neoplastic development in the mouse mammary gland, and suggest that EGF can mimic the ERM-NM-1-mediated effects of E in this organ. Gene expression of mammary gland organ culture and DMBA-induced lesions from 4 mouse strains.

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Transcription profiling of murine mammary glands to study early events occuring in p53-independent hormone-induced tumorigenesis

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