Breast Cancer

, Volume 17, Issue 2, pp 86–91

Prediction of hormone sensitivity for breast cancers

  • Yasuo Miyoshi
  • Keiko Murase
  • Masaru Saito
  • Koushi Oh
Special Feature Breast cancer research from bench to bedside

DOI: 10.1007/s12282-009-0177-x

Cite this article as:
Miyoshi, Y., Murase, K., Saito, M. et al. Breast Cancer (2010) 17: 86. doi:10.1007/s12282-009-0177-x

Abstract

The classic action that leads to transcriptional activation of estrogen response genes mediated through estrogen receptors (ER) and the estrogen complex plays a pivotal role in the development of ER-positive breast cancers. In addition to this pathway, non-classic action and non-genomic action, both estrogen-dependent and estrogen-independent genomic actions have also been found to contribute to ER-positive tumor growth. Although the details of these mechanisms are not well known, participation of the growth factor signaling pathway is likely to be the most significant factor for acquisition of resistance to hormonal therapy. This resistance is mediated not only directly through cell growth promotion by growth factor signaling, but also through enhancement of alternative ER signaling pathways in addition to classic action. The reason why tamoxifen-insensitive ER-positive breast cancers respond to aromatase inhibitors may be explained, at least in part, by the different estrogen-related signaling pathways in which aromatase inhibitors may block estrogen signaling. In this paper we discuss the molecular mechanisms for resistance to hormonal therapy based on an understanding of estrogen signaling pathways.

Keywords

Breast cancerSignaling pathwayHormonal therapyGrowth factor

Copyright information

© The Japanese Breast Cancer Society 2009

Authors and Affiliations

  • Yasuo Miyoshi
    • 1
  • Keiko Murase
    • 1
  • Masaru Saito
    • 1
  • Koushi Oh
    • 1
  1. 1.Division of Breast and Endocrine Surgery, Department of SurgeryHyogo College of MedicineNishinomiyaJapan