Abstrait
Le développement du trastuzumab, anticorps monoclonal humanisé anti-HER2, a débuté en 1984 avec ľidentification de ľoncogène HER2 (1), rapidement suivie par son clonage (2, 3) et par la démonstration qu’un anticorps monoclonal dirigé contre le produit de ľoncogène — en ľoccurrence le récepteur HER2 — pouvait inhiber la croissance des cellules transformées HER2 (4). Dans le même temps, la recherche translationnelle prouvait la corrélation entre ľamplification du gène HER2, présente dans 25 à 30% des cancers du sein, et un mauvais pronostic (5). Ľimpact clinique a été établi dès 2001, en phase métastatique, avec une amélioration de la survie des patientes avec cancer du sein HER2 positif grâce à la combinaison avec la chimiothérapie (6), et confirmé de façon particulièrement impressionnante en phase adjuvante en 2005 avec les résultats de cinq études randomisées distinctes (7–10), permettant toutes ďobtenir une réduction du risque relatif de rechute de 50%, chiffre rarement atteint dans ľhistoire des essais adjuvants pour le cancer mammaire. Ces cinq études cliniques adjuvantes publiées ou rapportées, c’est-à-dire ľétude HERA (7, 8), ľanalyse poolée (9) des deux études nord-américaines NSABP-B31 et NCCTG/N9831, ľétude BCIRG 006 (10, 11) et ľétude FinHER (12), sont analysées et discutées dans ce chapitre.
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Bernard-Marty, C., Piccart-Gebhart, M. (2007). Traitement adjuvant et cancer du sein surexprimant HER2. In: Le cancer du sein. Oncologie pratique. Springer, Paris. https://doi.org/10.1007/978-2-287-36073-2_10
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DOI: https://doi.org/10.1007/978-2-287-36073-2_10
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