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| Antihuman epidermal growth factor receptor 2 (HER2) monoclonal antibody trastuzumab enhances cytolytic activity of class I-restricted HER2-specific T lymphocytes against HER2-overexpressing tumor cells |
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| Author(s): zum Buschenfelde CM, Hermann C, Schmidt B, Peschel C, Bernhard H |
| Source: CANCER RESEARCH Volume: 62 Issue: 8 Pages: 2244-2247 Published: APR 15 2002 |
| Times Cited: 41 References: 20 |
| Abstract: The monoclonal antibody trastuzumab (Herceptin) directed against the human epidermal growth factor receptor 2 (HER2) results in tumor regressions when administered to patients with HER2-overexpressing breast cancer. One of the underlying mechanisms of this antibody-induced tumor regression is based on the internalization and degradation of HER2 by tumor cells on interaction with trastuzumab. subsequently inhibiting signal transduction pathways. As antibody-induced degradation of HER2 is likely to be accompanied with increased numbers of HER2 peptides presented with MHC. we asked whether trastuzumab-treated tumor cells were more susceptible to CTL-mediated lysis. Here we show that the cytolytic activity of human, HER2-specific CD8(+) CTLs is augmented by anti-HER2 antibody, trastuzumab. HER2-reactive CTL clones lyse class I-matched, HER2-overexpressing tumor cells more efficiently after treatment with trastuzumab. The potentially synergistic activity of HER2-specific antibody and CTL encourages the development of an HER2-targeted immunotherapy using a combination of inhibitory antibodies and CTLs for patients with HER2-overexpressing tumors. |
| Document Type: Article |
| Language: English |
| Reprint Address: Bernhard, H (reprint author), Tech Univ Munich, Klinikum Rechts Isar, Med Klin, Dept Hematol Oncol, Ismaningerstr 22, D-81675 Munich, Germany |
Addresses:
1. Tech Univ Munich, Klinikum Rechts Isar, Med Klin, Dept Hematol Oncol, D-81675 Munich, Germany |
| Publisher: AMER ASSOC CANCER RESEARCH, PO BOX 11806, BIRMINGHAM, AL 35202 USA |
| Subject Category: Oncology |
| IDS Number: 543ML |
| ISSN: 0008-5472 |
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