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Caveolin-1, mammary stem cells, and estrogen-dependent breast cancers.

Caveolin-1, mammary stem cells, and estrogen-dependent breast cancers. Research Abstract Details 

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  • Caveolin-1, mammary stem cells, and estrogen-dependent breast cancers. Abstract Text:

    federica sotgiaFederica Sotgia,hallgeir ruiHallgeir Rui,gloria bonuccelliGloria Bonuccelli,isabelle mercierIsabelle Mercier,richard g pestellRichard G Pestell,michael p lisantiMichael P Lisanti,

    Estrogen exposure is considered a significant risk factor for breast cancer development. Estrogen receptor (ER) alpha is expressed at low levels in normal epithelia, and its expression is dramatically up-regulated as transformation progresses during mammary hyperplasia and adenocarcinoma development. The mechanism(s) driving ERalpha up-regulation during mammary tumorigenesis remains unclear. Caveolin-1 (Cav-1) is the structural protein of plasmalemmal invaginations, termed caveolae, which functions as a tumor suppressor gene. Interestingly, Cav-1 dominant-negative mutations are exclusively found in ERalpha-positive breast cancer samples. In support of these clinical findings, ERalpha expression is increased in Cav-1 (-/-) null mammary epithelia, and estrogen stimulation further enhances the growth of Cav-1-deficient three-dimensional epithelial structures. These phenotypes correlate with augmented levels of cyclin D1. In addition, Cav-1 gene inactivation induces the accumulation of a cell population with the characteristics of adult mammary stem cells. Primary cultures of Cav-1 (-/-) mammary epithelial cells exhibit premalignant changes, such as abnormal lumen formation, epidermal growth factor-independent growth, defects in cell substrate attachment, and increased cell invasiveness. Thus, Cav-1 gene inactivation promotes premalignant alterations in mammary epithelia and induces increased ERalpha expression levels and the up-regulation of cyclin D1. As tumor formation is a multihit process, Cav-1 mutations that occur during the early stages of mammary transformation may be a critical upstream/initiating event leading to increased ERalpha levels.

    Caveolin-1, mammary stem cells, and estrogen-dependent breast cancers. Publishing Authors By Initials

    f sotgiaF Sotgia,h ruiH Rui,g bonuccelliG Bonuccelli,i mercierI Mercier,rg pestellRG Pestell,mp lisantiMP Lisanti,

    For similar neoplasms: neoplasms, hormone-dependent research abstracts see: neoplasms: neoplasms, hormone-dependent research

    PUBMED ID PMID:

    MEDLINE DATE:

    Caveolin-1, mammary stem cells, and estrogen-dependent breast cancers. Journal Published:

    PUBLICATION TYPE: Review

    Journal: Cancer research

    VOLUME: 66

    Page Numbers: 10647-51

    Journal Abbreviation: Cancer Res.

    ISSN: 0008-5472

    DAY: 15

    MONTH: Nov

    YEAR: 2006

    Caveolin-1, mammary stem cells, and estrogen-dependent breast cancers. Information

    Number of References: 41

    LANGUAGE: eng

    NlmUniqueID: 2984705

    Caveolin-1, mammary stem cells, and estrogen-dependent breast cancers. Keywords Mesh Terms:

    KEYWORDS: Neoplasms, Hormone-Dependent

    MESH TERMS: pathology

    Chemical & Substance for Abstract: Caveolin-1, mammary stem cells, and estrogen-dependent breast cancers. Information

    Substance Name: Estrogen Receptor alpha

    Registry Number: 0

    Grant and Affiliation Information for Caveolin-1, mammary stem cells, and estrogen-dependent breast cancers.

    AFFILIATION: Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NCI

    GRANT: R01CA98779

    ACRONYM: CA

    MEDLINETA: Cancer Res

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

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