A role for the pseudokinase HER3 in the acquired resistance against EGFR- and HER2-directed targeted therapy

Jeroen Claus*, Gargi Patel, Tony Ng, Peter Parker

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)

Abstract

Specific inhibition of members of the EGFR (epidermal growth factor receptor) family, particularly EGFR and HER2 (human epidermal growth factor receptor 2), are an important therapeutic strategy in many human cancers. Compared with classical chemotherapy, these targeted therapeutics are very specific and initially effective, but acquired resistance against these targeted therapies is a recurring threat. A growing body of recent work has highlighted a pseudokinase in the EGFR family, HER3, and its ligand, NRG (neuregulin flu), to be of importance in models of resistant cancers, as well as in patients. In the present article, we describe some of the roles in which HER3 can mediate acquired resistance and discuss the current efforts to target HER3 itself in cancer.

Original languageEnglish
Pages (from-to)831-836
Number of pages6
JournalBiochemical Society Transactions
Volume42
Issue number4
DOIs
Publication statusPublished - Aug 2014

Keywords

  • cancer
  • drug resistance
  • epidermal growth factor receptor (EGFR)
  • human epidermal growth factor receptor 2 (HER2)
  • human epidermal growth factor receptor 3 (HER3)
  • kinase inhibition
  • CLINICAL-PRACTICE GUIDELINES
  • GROWTH-FACTOR RECEPTOR
  • BREAST-CANCER CELLS
  • LUNG-CANCER
  • FOLLOW-UP
  • KINASE INHIBITORS
  • AXL KINASE
  • ACTIVATION
  • DIAGNOSIS
  • ERBB3

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