Fig. 3

Mechanism of action of AVEC: anti-HER-2 × HBsAg. a SK-BR-3 breast cancer cells were labeled for 1–7 h at 37 °C with 0.3 mg/ml trastuzumab or anti-HER-2 × HBsAg in full human sera from the HBV—vaccinated patients keeping 10.0 IU/ml anti-HBV. That was followed by studying growth inhibition through thymidine incorporation, b The breast cancer cells from the patient with metastatic HER-2⁺ breast cancer were treated as in (a) including fluorescent AVEC: anti-HER-2 x HBsAg, labeling with anti-phosphatidylserine (anti-PS) to detect apoptosis or propidium iodide (PI) to detect necrosis. These tests were repeated three times. This route of MOA is representative for all 10 patients’ breast cancer cells. After 1 h only a few cells were showing signs of chromatin collapse. After 6 h most of the cells, which were marked as apoptotic by anti-PS (c) were also necrotic. Almost 40 % of the cancer cells were apoptotic due to treatment. That more than doubled due to the treatment with anti-HER-2₀₀₁ × HBsAg or anti-HER-2₀₀₄ × HBsAg. Nearly 10 % were determined necrotic as the result of the treatment with trastuzumab (d). The percentage of the necrotic cells due to the treatment with anti-HER-2₀₀₁ × HBsAg or anti-HER-2₀₀₄ × HBsAg more than tripled over that attained with trastuzumab