STAT1-deficient mice spontaneously develop estrogen receptor α-positive luminal mammary carcinomas.

ABSTRACT:

Introduction

Although breast cancers expressing estrogen receptor-α (ERα) and progesterone receptors (PR) are the most common form of mammary malignancy in humans, it has been difficult to develop a suitable mouse model showing similar steroid hormone responsiveness. STAT transcription factors play critical roles in mammary gland tumorigenesis, but the precise role of STAT1 remains unclear. Herein, we show that a subset of human breast cancers display reduced STAT1 expression and that mice lacking STAT1 surprisingly develop ERα+/PR+ mammary tumors.

Methods

We used a combination of approaches, including histological examination, gene targeted mice, gene expression analysis, tumor transplantaion, and immunophenotyping, to pursue this study.

Results

Forty-five percent (3

SUBMITTER: Chan SR 

PROVIDER: S-EPMC3496133 | biostudies-literature | 2012 Jan

REPOSITORIES: biostudies-literature