Abstract
Anti-HER2/neu antibody therapy is reported to mediate tumor regression by interrupting oncogenic signals and/or inducing FcR-mediated cytotoxicity. Here, we demonstrate that the mechanisms of tumor regression by this therapy also require the adaptive immune response. Activation of innate immunity and T cells, initiated by antibody treatment, was necessary. Intriguingly, the addition of chemotherapeutic drugs, although capable of enhancing the reduction of tumor burden, could abrogate antibody-initiated immunity leading to decreased resistance to rechallenge or earlier relapse. Increased influx of both innate and adaptive immune cells into the tumor microenvironment by a selected immunotherapy further enhanced subsequent antibody-induced immunity, leading to increased tumor eradication and resistance to rechallenge. This study proposes a model and strategy for anti-HER2/neu antibody-mediated tumor clearance.
Original language | English (US) |
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Pages (from-to) | 160-170 |
Number of pages | 11 |
Journal | Cancer Cell |
Volume | 18 |
Issue number | 2 |
DOIs | |
State | Published - Aug 2010 |
Keywords
- Cellcycle
- Cellimmuno
- Molimmuno
ASJC Scopus subject areas
- Oncology
- Cancer Research