Next-generation sequencing analysis of control mammary glands and ECD transgenic tumors
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ABSTRACT:
PROVIDER: PRJNA826889 | ENA |
REPOSITORIES: ENA
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Project description: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. Keywords: disease state analysis
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Project description:Many components of Wnt/β-catenin signaling pathway also play critical roles in mammary tumor development. To study the role of Apc in mammary tumorigensis, we introduced conditional Apc mutations specifically into two different mammary epithelial populations using K14-Cre (progenitor) and WAP-cre (lactaing luminal) transgenic mice. Only the K14-cre mediated Apc heterozygosity developed mammary adenocarcinomas demonstrating histological and molecular heterogeneity, suggesting the progenitor cell origin of these tumors. These tumors harbored truncation mutation in a very defined region in the remaining wild-type allele of Apc that would retain some down-regulating activity of β-catenin signaling. Our results suggest that not only the epithelial origin but also a certain Apc mutations are selected to achieve a specific level of β-catenin signaling optimal for mammary tumor development.
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