Prostate cancer: 11. Alternative approaches and the future of treatment
| Table 1: New biological strategies for the treatment of prostate cancer | |
| Strategy | Mechanism |
| Anti-angiogenesis | Tumour growth depends on new blood vessels. Tumour cells secrete growth factors (e.g., vascular endothelial growth factor) that bind to receptors on endothelial cells to stimulate their proliferation. Some agents interrupt this pathway. |
| Inhibition of growth-factor receptors on tumour cells | Malignant cells (including those in prostate tumours) depend on stimulating growth factors that bind to specific receptors. Some agents prevent such binding. |
| Differentiation therapy | Cancer cells may undergo tissue-specific differentiation or proliferation. Some agents stimulate differentiation and inhibit proliferation. |
| Stimulation of apoptosis | Apoptosis (programmed cell death) occurs after androgen withdrawal in hormone-sensitive prostate cancer. Stimulation of the genes that promote apoptosis (e.g., bax) or antisense constructs to genes that inhibit it (e.g., bcl2) might cause cell death in hormone-refractory prostate cancer. |
| Immunologic approaches | Recent advances in our understanding of the molecular complexity of the immune system allow new approaches including the isolation and cultivation of a patient’s own antigen-presenting cells (dendritic cells) followed by reinfusion. |
| Gene therapy | Various genes can cause death of the cells into which they are introduced, either directly or by stimulating immune mechanisms. The key to this approach is to develop strategies that allow insertion of specific genes into prostate cancer cells. One method is to use viruses that seek cells producing prostate-specific antigen to insert these "suicide" genes. |
