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Summary: Cav-1 functional inactivation in mammary tumorigenesis. Cav-1 inactivation (either by loss-of-function mutations or by genetic ablation) in mammary epithelial cells induces increases in ER levels, correlating with enhanced estrogen sensitivity. Up-regulation of ERα promotes the growth of Cav-1-deficient acini and increases cyclin D1 levels. Thus, our results suggest a novel pathway leading toward mammary tumorigenesis.
