Formation of Neu/ErbB2-induced mammary tumors is unaffected by loss of ErbB4

A. J. Jackson-Fisher, G. Bellinger, E. Shum, J. K. Duong, A. S. Perkins, M. Gassmann, W. Muller, Kevin C K Lloyd, D. F. Stern

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


The four members of the ErbB family of receptor tyrosine kinases are involved in development and tumorigenesis of the mammary gland. Whereas the epidermal growth factor receptor, ErbB2 and ErbB3 are positively associated with various cancers, clinical studies of ErbB4 in breast cancer are contradictory. Results from tissue culture analyses and some clinical studies suggested that ErbB4 is either a tumor suppressor or is a negative regulator of ErbB2-driven tumors. Neu-Cre-ErbB4flox/null mice in which ErbB4 was inactivated by Cre-lox-mediated recombination in the mammary gland developed MMTV-Neu-driven mammary tumors with a similar latency period to mice with one or two wild-type ErbB4 alleles. Moreover, there was no difference in the histologies of tumors that developed, nor in the propensity to form lung metastases. Taken together these results suggest that ErbB4 is not a potent, highly penetrant tumor suppressor, nor is it a factor in Neu-mediated tumorigenesis in this model.

Original languageEnglish (US)
Pages (from-to)5664-5672
Number of pages9
Issue number41
StatePublished - Sep 14 2006


  • Breast cancer
  • Carcinoma
  • ErbB
  • HER-4
  • MMTV-Neu

ASJC Scopus subject areas

  • Molecular Biology
  • Cancer Research
  • Genetics


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