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Expression of mutant p53 in Mammary carcinomas in WAP-SV40 transgenic mice

ABSTRACT: Upon induction, WAP-T mice express two synergistically acting SV40 early region encoded proteins, large (LT) and small (sT) tumor antigens in the mammary epithelium, recapitulating thereby the loss of p53 and Rb function and deregulation of PP2A-controlled mitogenic pathways in human breast cancer. In primiparous mice, WAP-promoter driven expression of SV40 proteins induces well and poorly differentiated (respectively low- and high-grade) mammary adenocarcinomas. We here studied the postulated mutant p53 (mutp53) 'gain of function' during mammary tumor development, progression and metastasis by crossing WAP-T mice with mutant p53 transgenic WAP-mutp53 mice. This study includes gene expression analysis of 12 high grade mammary carcinoma samples. An alternative probe set mapping published by the AffyProbeMiner project (remapped transcript consistent cdf-file) was used to calculate probe set signals of 6 mono-trangenic WAP-T-NP8 samples from the dataset GSE29117 and 6 bi-transgenic WAP-T-NP8 x WAP-W10 (mutp53R245R) samples.

ORGANISM(S): Mus musculus

SUBMITTER: Florian Wegwitz

PROVIDER: E-GEOD-53395 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression of mutant p53 in Mammary carcinomas in WAP-SV40 transgenic mice

Project description:Upon induction, WAP-T mice express two synergistically acting SV40 early region encoded proteins, large (LT) and small (sT) tumor antigens in the mammary epithelium, recapitulating thereby the loss of p53 and Rb function and deregulation of PP2A-controlled mitogenic pathways in human breast cancer. In primiparous mice, WAP-promoter driven expression of SV40 proteins induces well and poorly differentiated (respectively low- and high-grade) mammary adenocarcinomas. We here studied the postulated mutant p53 (mutp53) 'gain of function' during mammary tumor development, progression and metastasis by crossing WAP-T mice with mutant p53 transgenic WAP-mutp53 mice.

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Mammary carcinomas in WAP-SV40 transgenic mice

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Mammary carcinomas in WAP-SV40 transgenic mice [gene expression]

Project description:Transgenic expression in mice of two synergistically acting SV40 early region encoded proteins, large (LT) and small (sT) tumor antigens, in the mammary epithelium recapitulates loss of p53 and Rb function and deregulation of PP2A-controlled mitogenic pathways in human breast cancer. In primiparous mice, WAP-promoter driven expression of SV40 proteins induces well and poorly differentiated mammary adenocarcinomas. We performed a correlative aCGH and gene expression analysis of 25 monofocal tumors, representing four histopathological grades, to explore the molecular traits of SV40-induced mammary tumors and to emphasize the relevance of this tumor model for human breast tumorigenesis. Gene expression analysis of 25 mammary carcinoma samples of two different WAP-SV40 mouse lines, T1 and NP8. Three involuted mammary gland tissues were included in the study as reference samples.

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Mutant p53 Increases Incidence and Promotes Progression of Mammary Carcinomas in Mice

Project description:In human breast cancer, mutations in the p53 gene are associated with poor prognosis, suggesting a mutant p53 “gain of function”. To study this phenomenon, we co-expressed mutant p53R270H in mice in which SV40 early proteins initiate the development of mammary adenocarcinomas in descendants of mammary epithelial cells that survived involution (WAPT-mice). This model allows the characterization of mammary carcinomas that developed in the absence or presence of mutant p53, while the endogenous wild-type p53 is functionallycompromised. Co-expression of mutant p53 significantly aggravated the phenotype of bitransgenic mice, as evidenced by a higher tumor incidence, a worse clinical staging and histological grading, as well as an enhanced invasiveness of the tumors, and more frequent pulmonary metastasis. Our data indicate that mutant p53 does not exert this effect by increasing genomic instability. On the contrary, lower grade tumors in WAP-T mice generally accumulated more amplifications of pro-survival genes than the corresponding tumors in bitransgenic animals, suggesting that mutant p53 can compensate for such genetic alterations by alternative mechanisms, possibly by its transcriptional activities, and thereby facilitate tumor formation. As a common feature and associated with their enhanced invasiveness, high grade tumors showed high level amplification of the Met-locus. Keywords: mutant p53, SV40 early proteins, tumor progression, tumor grade, tumor stage, mammary carcinoma, animal model, Met

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Project description:Mammary carcinomas in WAP-SV40 transgenic mice

| PRJNA145965 | ENA