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Myc and Mammary Cancer: Myc is a Downstream Effector of the ErbB2 Receptor Tyrosine Kinase

Hynes, Nancy ; Lane, Heidi

In: Journal of Mammary Gland Biology and Neoplasia, 2001, vol. 6, no. 1, p. 141-150

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    Titre
    • Myc and Mammary Cancer: Myc is a Downstream Effector of the ErbB2 Receptor Tyrosine Kinase
    Auteur
    • Hynes, Nancy. Friedrich Miescher Institute, PO Box 2543, CH-4002, Basel, Switzerland
    • Lane, Heidi. Novartis Pharma, K-125.1317, CH-4002, Basel, Switzerland
    Type de document
    • Postprint
    Langue
    • Inglese
    Publié dans
    • Journal of Mammary Gland Biology and Neoplasia, 2001, vol. 6, no. 1, p. 141-150. Kluwer Academic Publishers-Plenum Publishers
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:319707
    Summary
    The proto-oncogene c-myc encodes a transcription factor which plays a major role in the regulation of normal cellular proliferation and is aberrantly expressed in many breast tumors. In a normal cell Myc expression levels are tightly regulated being subject to many layers of control. Errantly expressed Myc collaborates with other oncogenes to promote transformation. In this review we will focus on the association between abnormal Myc expression and mammary cancer. In particular, we will discuss the role of Myc as a downstream effector of the ErbB2 receptor tyrosine kinase which is overexpressed and constitutively activate in many mammary tumors. The cooperation between Myc and ErbB2 in transformation will be discussed in relation to clinical studies on Myc in human cancer and with consideration of transgenic models of Myc-induced mammary cancer. Data from our laboratory will be presented showing that deregulated ErbB2 activity strongly stimulates cytoplasmic signaling pathways which in turn impinge on Myc at multiple levels causing its deregulated expression