Almost 25 years ago we first employed antisense oligonucleotides (oligos) against human derived prostatic LNCaP cells using both in vitro [1] and in vivo [2] models; initially targeting the epidermal growth factor receptor, and its ligand, transforming growth factor-alpha. Similar studies and results were found when we treated in vitro and in vivo breast cancer models [3]. Clinically, oligos have been employed to treat cancer patients (including those with prostate tumors), targeting apoptosis

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... nhibitors (bcl-2, clusterin) in attempts to restore tumor chemo-[4] or radio-sensitivity [5]. Yet, in spite of these patient trials and additional advances in early detection of prostate cancer, its treatment has not greatly improved in recent years. In the last few years gene therapy and newly discovered immune checkpoint blockade has given some indication that they could provide some additional improvement, particularly when administered following surgery, chemotherapy or irradiation. Volume 2 | Issue 3 | 2 of 9 Cancer Sci Res, 2019 of promoters, while other mechanisms which facilitate apoptosis may be enhanced. This study suggests that compensatory changes in the regulation of apoptosis can vary or be limited to apoptosis promoters (caspase-3), since the expression of the non-targeted apoptosis inhibitor clusterin is not affected and there is suggestion that the activator of apoptosis VDCA1 could be enhanced. Should bcl-2 suppression be clinically employed with antisense oligos it may require maintenance (or replacement) of caspase-3 activity.