Founded in 1993
  Year: 2006 | Volume: 14 | Issue: 3-4 | Pages: 146-150
  Review Article
Todorovic-Rakovic N, Neskovic-Konstantinovic Z, Nikolic-Vukosavljevic D.
  DOI: 10.2298/AOO0604146T
  In tumors in which estrogen receptor (ER) and growth factor signaling pathways are simultaneously active, there is a bidirectional cross-talk that results in a positive feedback cycle of cell survival and proliferation stimuli. Beside the postulated inverse correlation between ER and HER2 (human epidermal growth factor receptor 2) as a consequence of repressive feedback signaling loop, there are also other mechanisms regarding ER-HER2 interactions. It seems that MAPK (mitogen-activated protein kinase) pathway has a central role in synergistic action between ER and HER2 in normal mammary gland development, as well in the breast cancer. MAPK pathway is hyperstimulated in cells that overexpress HER2 as a consequence of HER2 gene amplification. In ER+ tumors, MAPK phosphorylates and activates either ER itself or ER coregulators, enhancing the transcriptional activation potential of ER. ER and HER2 signaling could interact on multiple levels (genomic or non-genomic) and therefore might induce reduced ER expression or might increase ER function. Based on our own research, dominant effect of postulated cross-talk was not related to HER2- induced reduced expression of ER (no difference in quantitative levels of ER in ER+ tumors regarding their HER2 status and no difference in progression-free time between ER+HER2- and ER+HER2+ patients) as presented. The importance of understanding ER-HER2 cross-talk is not only because of its significance in breast cancer progression, but because it seems to be fundamental factor.
  Key words: Breast Neoplasms; Receptors, Estrogen; Receptor, Epidermal Growth Factor; Receptor, erbB-2; Receptor Cross-Talk
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Founder and owner: Oncology Institute of Vojvodina, Serbia
Publisher: Oncology Institute of Vojvodina
Co-publisher: Faculty of Medicine, University of Novi Sad
Online since 1997 (Abstracts only); 2000 (Abstracts and Full text)
ISSN: 0354-7310 eISSN: 1450-9520