William R. Gwin III, MD, discusses the mechanism of action of alpha-tocopheryloxyacetic acid in HER2-positive metastatic breast cancer.
William R. Gwin III, MD, acting instructor at the Seattle Cancer Care Alliance and acting instructor of the Tumor Vaccine Group at the University of Washington School of Medicine, discusses the mechanism of action of alpha-tocopheryloxyacetic acid (α-TEA) in HER2-positive metastatic breast cancer.
It is understood that type 1 (Th1) cells are needed in order to generate antitumor immunity, says Gwin. Unfortunately, Th1 cells are lost in many tumors, adds Gwin. α-TEA appears to augment Th1 immunity by increasing CD4+ Th1 and CD8+ tumor-infiltrating lymphocyte levels and by boosting cytokines associated with Th1, such as interferon gamma.
α-TEA has been reported to augment TH1 immunity through an increase of activated effector memory CD4+ and CD8+ T cells and a decrease of immune suppressive CD4+CD25+ regulatory T cells in the tumor, says Gwin. These results suggest that the agent does mediate antitumor effects, but through the use of different mechanisms: through the generation of reactive oxygen species leading to apoptosis and through an immune-mediated component that drives the augmentation of the effectiveness of CD4+ and CD8+ cells, concludes Gwin.