Pathways driving the endocytosis of mutant and wild-type EGFR in cancer

Kaia K. Hampton, Rolf J. Craven

Research output: Contribution to journalArticlepeer-review

26 Scopus citations

Abstract

EGFR (epidermal growth factor receptor) is activated through changes in expression or mutations in a number of tumors and is a driving force in cancer progression.EGFR is targeted by numerous inhibitors, including chimeric antibodies targeting the extracellular domain and small molecule kinase domain inhibitors.The kinase domain inhibitors are particularly active against mutant forms of the receptor, and subsequent mutations drive resistance to the inhibitors.Here, we review recent developments on the trafficking of wild-type and mutant EGFR, focusing on the roles of MIG6, SPRY2, ITSN, SHP2, S2RPGRMC1 and RAK.Some classes of EGFR regulators affect wild-type and mutant EGFR equally, while others are specific for either the wild-type or mutant form of the receptor.Below we summarize multiple signalingassociated pathways that are important in trafficking wild-type and mutant EGFR with the goal being stimulation of new approaches for targeting the distinct forms of the receptor.

Original languageEnglish
Pages (from-to)504-512
Number of pages9
JournalOncoscience
Volume1
Issue number8
DOIs
StatePublished - 2014

Bibliographical note

Funding Information:
This research was funded in part by a grant from the Bonnie J Addario Lung Cancer Research Foundation.

Keywords

  • Endocytosis
  • Kinase
  • Receptor
  • Signaling
  • Therapeutics

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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