P95 HER2 fragments and breast cancer outcome. Issue 9 (September 2014)

• Record Type: Journal Article
• Authors: Tural, Deniz; Akar, Emre; Mutlu, Hasan; Kilickap, Saadettin
• Is Part Of: Expert review of anticancer therapy. Volume 14:Issue 9(2014)
• Page Start: 1089
• Page End: 1096
• Publication Date: 2014-09
• Subjects: Cancer -- Treatment -- Periodicals; 616.99406
• DOI: 10.1586/14737140.2014.929946
• Languages: English
• ISSNs: 1473-7140

Abstract

<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <p>HER2 is a 185-kDa transmembrane oncoprotein encoded by the <italic>HER2</italic> gene. It is located on chromosome 17q21 and is overexpressed in approximately 15% of invasive breast cancers. In addition, it is a poor prognostic factor for survival and disease progression. Approximately 30% of HER2-positive tumors also express a series of carboxy-terminal HER2 fragments known as p95HER2, in addition to the full-length HER receptor. Previous studies have found that p95HER2 represents an independent prognostic marker in patients with HER2-positive disease. Moreover, p95HER2 status might be a decisive factor when choosing between different therapies because p95HER2 fragment-positive tumors are resistant to trastuzumab but respond to tyrosine kinase inhibitors, such as lapatinib, as do p95HER2-negative tumors. p95HER2 fragments arise through at least two different mechanisms: proteolytic shedding of the full-length p185HER2 receptor extracellular domain and translation of <italic>HER2</italic> mRNA from internal initiation codons. The present review is based primarily on recent studies suggesting p95HER2 constitutes a new surrogate marker for an aggressive HER2-positive breast cancer subtype with distinct clinical and biological features.</p> </abstract>