title: [Breast cancer--known receptors, new pathways?].
abstract: The deregulation of receptor tyrosine kinases is an essentiell factor in die initiation and progression of malignant tumours. With the introduction of Herceptin in the adjuvant therapy of invasive breast cancer, the determination of the c-erbB2 expression status became an essential part in the workup of breast cancer biopsies. The commonly used diagnostic algorithm is based on a detailed knowledge about molecular mechanisms and downstream signal cascades. In contrast to c-erbB2, the underlying molecular mechanisms and potential predictive parameters, associated with the expression of the Epidermal Growth Factor Receptor (EGFR) are likewise unclear. With the introduction of anti-EGFR directed therapies in the treatment of malignant tumours, an improved knowledge about the role in the progression of breast cancers is urgently needed. This article will focus on important improvements in the knowledge of EGFR-overexpression in breast cancer cells, especially in the context of egfr-amplifications.
authors.affiliation: Gerhard-Domagk-Institut für Pathologie, Universität Münster.
authors.forename: Horst
authors.initials: H
authors.lastname: Bürger
mesh_terms: D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D001943:Breast Neoplasms / Q000188:drug therapy / Q000235:genetics / Q000473:pathology*; D066246:ErbB Receptors / Q000235:genetics*; D005260:Female; D005784:Gene Amplification; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000235:genetics; D000068878:Trastuzumab
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D066246:ErbB Receptors; D018719:Erb-b2 Receptor Tyrosine Kinases; D000068878:Trastuzumab