Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse mammary tumors from K14-cre; ApcCKO/+ vs control mammary glands


ABSTRACT: 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. Experiment Overall Design: We have compared 3 mammary tumors from K14-cre; ApcCKO/+ mice with 3 control mammary glands.

ORGANISM(S): Mus musculus

SUBMITTER: Dmitriy Sonkin 

PROVIDER: E-GEOD-14753 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Genetic mechanisms in Apc-mediated mammary tumorigenesis.

Kuraguchi Mari M   Ohene-Baah Nana Yaw NY   Sonkin Dmitriy D   Bronson Roderick Terry RT   Kucherlapati Raju R  

PLoS genetics 20090206 2


Many components of Wnt/beta-catenin signaling pathway also play critical roles in mammary tumor development, yet the role of the tumor suppressor gene APC (adenomatous polyposis coli) in breast oncongenesis is unclear. To better understand the role of Apc in mammary tumorigenesis, we introduced conditional Apc mutations specifically into two different mammary epithelial populations using K14-cre and WAP-cre transgenic mice that express Cre-recombinase in mammary progenitor cells and lactating lu  ...[more]

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