Cross-talk between the ErbB/HER family and the type I insulin-like growth factor receptor signaling pathway in breast cancer

Quanri Jin, Francisco J. Esteva

Research output: Contribution to journalArticle

114 Scopus citations

Abstract

Understanding the molecular mechanisms involved in tumorigenesis and their influence on clinical outcome is providing specific molecular markers for targeted therapy. Activation of tyrosine kinase receptors from the human epidermal growth factor receptor family (EGFR, HER2, HER3, HER4) and the insulin-like growth factor receptor I (IGF-IR) plays a key role in the initiation and progression of breast cancer. HER2 overexpression is a validated therapeutic target, as shown by the clinical efficacy of trastuzumab and lapatinib. However, only 25-30% of patients with HER2-overexpressing tumors respond to single-agent trastuzumab or lapatinib, and resistance develops even in responding patients. Therefore, to optimize therapeutic efficacy, it is urgent to elucidate the complex network of signaling pathways that develop in breast cancer cells. Signaling interactions have been reported between ErbB/HER family members and IGF-IR. As increased IGF-IR signaling has been implicated in trastuzumab resistance, agents targeting HER2, and IGF-IR could be potential therapeutic tools in breast cancers that develop resistance to HER2-directed therapy.

Original languageEnglish (US)
Pages (from-to)485-498
Number of pages14
JournalJournal of Mammary Gland Biology and Neoplasia
Volume13
Issue number4
DOIs
StatePublished - Nov 26 2008

Keywords

  • Breast cancers
  • Human epidermal growth factor receptor
  • Insulin-like growth factor receptor
  • Signaling interactions

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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