par Bedard, Philippe L;Cardoso, Fatima 
;Piccart-Gebhart, Martine
Référence Journal of mammary gland biology and neoplasia, 14, 1, page (55-66)
Publication Publié, 2009-03
;Piccart-Gebhart, Martine Référence Journal of mammary gland biology and neoplasia, 14, 1, page (55-66)
Publication Publié, 2009-03
Article révisé par les pairs
| Résumé : | Although the development of trastuzumab and lapatinib has improved the outlook for women with HER-2 positive breast cancer, resistance to HER-2 targeted therapy is a growing clinical dilemma. Recent evidence indicates that the HER-2 pathway may play an important role in the maintenance of cancer stem cells (CSCs). The success of HER-2 targeted therapies may, in part, be explained by their direct activity against HER-2 positive CSCs. Our understanding of the mechanisms involved in resistance to trastuzumab, including loss or blockade of the trastuzumab binding site, activation of alternative signaling pathways, and induction of epithelial-mesenchymal transition (EMT), suggests that CSCs may be at the root of resistance of HER-2 targeted therapy. A variety of novel HER-2 targeted approaches have demonstrated promising preliminary clinical activity. Future clinical trials should involve the integration of technologies to assess the impact of novel HER-2 targeted therapies on HER-2 positive CSCs. |
