Novel approaches to target HER2-positive breast cancer: trastuzumab emtansine

The human epidermal growth factor receptor 2 (HER2) is overexpressed in 20% of breast carcinomas. Prior to the development of targeted therapies, HER2-positive breast cancer was associated with more aggressive disease and poor prognosis. Trastuzumab emtansine (T-DM1) is an antibody-drug conjugate th...

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Bibliographic Details
Published in:Cancer management and research 2016-01, Vol.8 (Issue 1), p.57-65
Main Authors: Recondo, Jr, Gonzalo, de la Vega, Maximo, Galanternik, Fernando, Díaz-Cantón, Enrique, Leone, Bernardo Amadeo, Leone, José Pablo
Format: Article
Language:English
Subjects:
Apoptosis
Breast cancer
Cancer therapies
Cell cycle
Chemotherapy
Cytotoxicity
Drug dosages
Epidermal growth factor
Genetic aspects
HER2 receptor
HER2-positive Breast Cancer
Kinases
Ligands
Medical prognosis
Metastasis
Metastatic Breast Cancer
Monoclonal antibodies
Patients
Prognosis
Review
T-DM1
Targeted cancer therapy
Targeted Therapies
Trastuzumab Emtansine
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Summary:The human epidermal growth factor receptor 2 (HER2) is overexpressed in 20% of breast carcinomas. Prior to the development of targeted therapies, HER2-positive breast cancer was associated with more aggressive disease and poor prognosis. Trastuzumab emtansine (T-DM1) is an antibody-drug conjugate that results from the combination of trastuzumab and DM1, a derivative of the antimicrotubule agent maytansine. This molecule has the ability to enhance cytotoxic drug delivery to specifically targeted cells that overexpress HER2, therefore, maximizing efficacy while sparing toxicity. In recent years, T-DM1 has shown to improve outcomes in metastatic HER2-positive breast cancer that is resistant to trastuzumab. In addition, T-DM1 is currently being tested in the neoadjuvant and adjuvant settings to identify patients who may benefit from this therapy. This review focuses on the mechanism of action, early and late-phase clinical trials, and ongoing studies of T-DM1 in HER2-positive breast cancer.
ISSN:1179-1322
1179-1322
DOI:10.2147/CMAR.S104447