Table 1.
Anti‐cancer strategy | Common agents | Mechanism of action | Advantages | References |
---|---|---|---|---|
Oncolytic viruses | Adenovirus; Measles virus; Herpes simplex virus |
Viruses infect, replicate in, and lyse tumor cells | Amplification of anti‐tumor effect with multiple rounds of infection; Selective replication in tumor cells |
75, 76, 77, 78, 98 |
Tumor‐ or tissue‐specific prodrugs | CD + 5‐5‐FU; Hsv‐tk + Ganciclovir; PSA‐activated thapsigargin peptide |
Cytotoxic drug metabolites induce cell death by inhibiting DNA synthesis (5‐FU, ganciclovir) or by inducing ER stress (thapsigargin) | Selective drug activation in tumor microenvironment | 79, 80, 81, 82, 83, 84 |
Immunomodulatory agents | IL‐2; IL‐12; Interferon‐β; CX3CL1 |
Lymphocyte activation and induction of tumor‐specific T‐cell responses; Direct induction of tumor cell differentiation and growth arrest | Endogenous signaling molecules; Potential direct and indirect effects on tumor growth; Synergy with other immunotherapies |
73, 89, 90, 91, 92 |
Apoptosis‐inducing agents | TRAIL | Direct induction of apoptosis via death receptors | Currently in clinical trials; Endogenous signaling molecule |
93, 94, 95, 96, 97 |
Cytotoxic chemotherapy | Paclitaxel; Doxorubicin |
Induction of cell death via inhibition of microtubule depolymerization (paclitaxel) or topoisomerase II function (doxorubicin) | FDA‐approved chemotherapeutic drugs |
68 |
Abbreviations: CD, cytosine deaminase; 5‐FU, 5‐fluoruracil; Hsv‐tk, herpes simplex virus‐thymidine kinase; PSA, prostate specific antigen; TRAIL, TNF‐related apoptosis‐inducing ligand.