Introduction One effective way to cure disease is to prevent the development of it all together. One modality to combat disease is cancer vaccines that would “program” an individual’s immune system to recognize foreign antigens by stimulating cytotoxic T lymphocytes (CTL) to attack cancer cells expressing a certain tumor antigen [1-5]. Current vaccine strategies to combat cancer include vaccines consisting of lymphocytes, which include: helper T lymphocytes (Th), dendritic cells (DC), macrophages, or reprogrammed oncolytic viruses [1,2]. Such vaccines may help deter cancer growth through stimulation of an individual’s immune system or by directly attacking a cancer growth [1]. Important questions arise when dealing with the idea of preventative cancer vaccines such as the practicality of utilizing vaccines to prevent the development of cancer as well as how many memory CTL’s need to be produced to provide a sentinel within an individual [1,6,7]. Cancer poses many issues to the vaccine development process as it displays the ability of antigen mimicry, a process by which tumor cells produce antigens with specific patterns of the host that can help cancer evade immune processing and development. Tumor antigen mimicry with self-antigen occurs since tumor-specific antigens (TSA) and tumorassociated (TAA) antigens are either mutated or overexpressed selfproteins, respectively (P53 and CEA). This results in active Th cells having a difficult time selecting for self from non-self. In addition, cancer growth displays variation; it may more rapid or slower than that of other disease processes. Such properties can result in a weak immune response. The multitude of complexities associated with cancer as well as its ability to deter host defenses has challenged researchers to seek for alternative therapies to chemotherapeutics due to their harmful side effects upon a host. One approach to treating cancer began in 1909 when the German scientist Paul Ehrlich proposed the “cancer immunosurveillance” hypothesis, which is the idea that the immune system can suppress an overwhelming number of carcinomas [4,8]. This approach was not tested until the 1950’s when the field of Immunology advanced. Experiments attempting to show support utilized mice that were inoculated with chemically-induced cancer cells; such cells lacked the capability to metastasize within a host. Over time, this led to the development of cancer-specific immunity in the recipient mice. This discovery provided the evidence needed for Ehrlich’s hypothesis. Such experiments demonstrated that it is essential to have the presence of an antigen to elicit an immune response in the host, because if no distinctive structures exist, then no recognition would be established [9]. F. Macfarlane Burnet and Lewis Thomas, well-known immunologists during the 20th century, hypothesized that for immunosurveillance to exist, lymphocytes would need to act aggressively akin to sentinels to recognize and eliminate a cancer threat. The cancer immunosurveillance theory revolves around three transitions states, denoted as “E’s” [9]:

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