Immunoexpression of HER family, neuregulin, MAPK and AKT in invasive ductal carcinomas of the breast

Eur J Gynaecol Oncol. 2008;29(4):350-6.

Abstract

Background: The purpose of this study was to investigate the frequency of expression of the erbB/HER family of growth factor receptors, their ligand neuregulinalpha (NRGalpha) and the most important pathways activated by HER receptors that are mitogen-activated protein kinase (MAPK) and serine/threonine kinase (AKT) in invasive ductal carcinomas of the breast, not otherwise specified (IDC-NOS).

Methods: 59 of the IDC-NOS of the breast were studied for ER, PR, EGFR, c-erbB-2, c-erbB-3, c-erbB-4, neuregulin Ab-3, phospho-AKT, and phospho-p44/42 map kinase using the streptavidin-biotin horseradish method.

Results: Of the 59 tumours, 44 (75%) were ER+, 37 (63%) PR+, four (7%) EGFR+, seven (12%) c-erbB-2+, seven (12%) c-erbB-3+ and 14 (24%) c-erbB-4+alpha. Strong cytoplasmic and/or nuclear immunoexpression was revealed in 17 (29%) cases for NRGalpha, 13 (22%) cases for p-AKT, and nuclear immunoexpression with p-MAPK was found in 17 (29%) cases.

Conclusion: The results suggest that high-grade breast carcinomas are not only associated with ER/PR- negativity, but seem to be activated by receptor tyrosine kinase growth factors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biomarkers, Tumor
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Carcinoma, Ductal, Breast / metabolism*
  • Carcinoma, Ductal, Breast / pathology
  • Carcinoma, Intraductal, Noninfiltrating / metabolism
  • Carcinoma, Intraductal, Noninfiltrating / pathology
  • ErbB Receptors / metabolism
  • Female
  • Humans
  • Immunohistochemistry
  • Mitogen-Activated Protein Kinases / metabolism*
  • Neuregulins / metabolism*
  • Protein-Tyrosine Kinases / metabolism
  • Receptors, Estrogen / metabolism
  • Receptors, Progesterone / metabolism

Substances

  • Biomarkers, Tumor
  • Neuregulins
  • Receptors, Estrogen
  • Receptors, Progesterone
  • ErbB Receptors
  • Protein-Tyrosine Kinases
  • Mitogen-Activated Protein Kinases