Table 3.
Molecular mechanisms underlying therapeutic efficacy of TA-specific mAb-based therapy.
| Immune effector cell-inpependent1 | Immune effector cell-dependent |
|---|---|
| Induce apoptosis | Activation of complement mediated: |
| Induce alteration in intracellular signaling | – phagocytosis |
| – complement-dependent cytotoxicity | |
| Inhibit growth factor binding to its cognate receptor | Trigger antibody dependent cellular cytotoxicity |
| Inhibit growth factor receptor activation | Induction of tumor cell necrosis or apopotsis leading to |
| – presentation of TA by APC | |
| – activation of CD(+) T cell mediated kill | |
| – activation of B cells and eosinophils | |
| – activation of TA-specific CTL |
1
Ultimately results in inhibition of cancer cell proliferation, tumor-induced angiogenesis, cancer cell invasion and metastasis, as well as potentating antitumor activity of cytotoxic drugs and radiotherapy