Trastuzumab Emtansine for Residual Invasive HER2-Positive Breast Cancer - Université de Montpellier
Article Dans Une Revue New England Journal of Medicine Année : 2019

Trastuzumab Emtansine for Residual Invasive HER2-Positive Breast Cancer

Gunter von Minckwitz
  • Fonction : Auteur
Chiun-Sheng Huang
  • Fonction : Auteur
Max Mano
  • Fonction : Auteur
Sibylle Loibl
  • Fonction : Auteur
Eleftherios Mamounas
  • Fonction : Auteur
Michael Untch
  • Fonction : Auteur
Norman Wolmark
  • Fonction : Auteur
Priya Rastogi
  • Fonction : Auteur
Andreas Schneeweiss
  • Fonction : Auteur
Andres Redondo
  • Fonction : Auteur
Hans Fischer
  • Fonction : Auteur
Alison Conlin
  • Fonction : Auteur
Claudia Arce-Salinas
  • Fonction : Auteur
Irene Wapnir
  • Fonction : Auteur
Christian Jackisch
  • Fonction : Auteur
Michael Digiovanna
  • Fonction : Auteur
Peter Fasching
  • Fonction : Auteur
John Crown
  • Fonction : Auteur
Pia Wülfing
  • Fonction : Auteur
  • PersonId : 874820
Zhimin Shao
  • Fonction : Auteur
Elena Rota Caremoli
  • Fonction : Auteur
Haiyan Wu
  • Fonction : Auteur
Lisa Lam
  • Fonction : Auteur
David Tesarowski
  • Fonction : Auteur
Melanie Smitt
  • Fonction : Auteur
Hannah Douthwaite
  • Fonction : Auteur
Stina Singel
  • Fonction : Auteur
Charles Geyer
  • Fonction : Auteur

Résumé

BACKGROUND: Patients who have residual invasive breast cancer after receiving neoadjuvant chemotherapy plus human epidermal growth factor receptor 2 (HER2)-targeted therapy have a worse prognosis than those who have no residual cancer. Trastuzumab emtansine (T-DM1), an antibody-drug conjugate of trastuzumab and the cytotoxic agent emtansine (DM1), a maytansine derivative and microtubule inhibitor, provides benefit in patients with metastatic breast cancer that was previously treated with chemotherapy plus HER2-targeted therapy. METHODS: We conducted a phase 3, open-label trial involving patients with HER2-positive early breast cancer who were found to have residual invasive disease in the breast or axilla at surgery after receiving neoadjuvant therapy containing a taxane (with or without anthracycline) and trastuzumab. Patients were randomly assigned to receive adjuvant T-DM1 or trastuzumab for 14 cycles. The primary end point was invasive disease-free survival (defined as freedom from ipsilateral invasive breast tumor recurrence, ipsilateral locoregional invasive breast cancer recurrence, contralateral invasive breast cancer, distant recurrence, or death from any cause). RESULTS: At the interim analysis, among 1486 randomly assigned patients (743 in the T-DM1 group and 743 in the trastuzumab group), invasive disease or death had occurred in 91 patients in the T-DM1 group (12.2%) and 165 patients in the trastuzumab group (22.2%). The estimated percentage of patients who were free of invasive disease at 3 years was 88.3% in the T-DM1 group and 77.0% in the trastuzumab group. Invasive disease-free survival was significantly higher in the T-DM1 group than in the trastuzumab group (hazard ratio for invasive disease or death, 0.50; 95% confidence interval, 0.39 to 0.64; P<0.001). Distant recurrence as the first invasive-disease event occurred in 10.5% of patients in the T-DM1 group and 15.9% of those in the trastuzumab group. The safety data were consistent with the known safety profile of T-DM1, with more adverse events associated with T-DM1 than with trastuzumab alone. CONCLUSIONS: Among patients with HER2-positive early breast cancer who had residual invasive disease after completion of neoadjuvant therapy, the risk of recurrence of invasive breast cancer or death was 50% lower with adjuvant T-DM1 than with trastuzumab alone. (Funded by F. Hoffmann-La Roche/Genentech; KATHERINE ClinicalTrials.gov number, NCT01772472 .).

Dates et versions

hal-02464524 , version 1 (03-02-2020)

Identifiants

Citer

Gunter von Minckwitz, Chiun-Sheng Huang, Max Mano, Sibylle Loibl, Eleftherios Mamounas, et al.. Trastuzumab Emtansine for Residual Invasive HER2-Positive Breast Cancer. New England Journal of Medicine, 2019, 380 (7), pp.617-628. ⟨10.1056/NEJMoa1814017⟩. ⟨hal-02464524⟩
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