The leading cancers among adult women and men are breast and prostate cancers, which affect nearly 130 people per 100,000 in the U.S. population (CDC, 2011), followed by cancers of the lung/bronchus and colon/rectum. The standard of care for the leading cancers comprises several therapeutic options, including surgery, pharmaceutical, hormonal, biological, and radiation. These approaches attempt to inhibit cancer cell growth through mechanisms including reduction or inhibition of tumor vascularization (anti-angiogenesis); promotion of apoptosis and interrupting cell cycle processes; and facilitating the body’s innate immune system to thwart and control cancer proliferation, possibly initiating cellular reprogramming and modulating checkpoint molecules and their ligands (CDC, 2011; Hewitt & Garlick, 2013; Naidoo et al., 2014).
Dietary interventions may preclude or reduce the risk of some forms of cancer. These interventions may function to attenuate inflammation through a series of intracellular events, including the phosphorylation or dephosphorylation of proteins and selected enzymes that impact cellular energetics and the expression of pro-inflammatory metabolites (Abrantes et al., 2014). Evidence suggests polyphenol metabolites from walnuts, almonds, and specific peach, plum, and cherry genotypes may function prophylactically in rodent and in vitro cancer models (Hardman, 2014; Evans-Johnson et al., 2013; Vizzotto et al., 2014). Certain strains of lactobacilli and bifidobacteria may moderate the risk of colorectal cancer by binding carcinogens and mutagens, decreasing cellular DNA damage, regulating DNA methylation in rectal mucosa, as well as signaling mucosal cells to produce an array of anticancer substances while modulating the immune system (Chong, 2014).
For more than 100 years, the medical and scientific communities have speculated on the etiology of malignant disease. Genetic markers and epigenetics, environmental factors, dietary patterns, personal lifestyles, and one’s immune status are among the many contributing factors to the development of cancer. Research during the 19th century, which marked the beginning of scientific oncology, suggested an association between selected viruses and tumorigenesis in several animal models. Anthropological evidence from ancient Egypt, China, and India indicated the presence of cancer-like disease that may have its roots in primitive viruses (Sarid and Gao, 2011; Javier & Butel, 2008). According to the International Agency for Research on Cancer, there are six human viruses classified as “carcinogenic to humans” (Bouvard et al., 2009). Those viruses include Epstein Barr virus, hepatitis B virus, human papilloma virus, human T-cell lymphotropic virus type 1, hepatitis C virus, and Kaposi sarcoma virus. A cell culture model system of the Epstein Barr virus, which has infected more than 95% of the population, can impact four biological processes, namely immune modulation, apoptosis regulation, cell proliferation, and genetic instability (McLaughlin-Drubin & Münger, 2008). Some speculate that these viruses contribute to approximately 15% to 20% of the global cancer burden (McLaughlin-Drubin & Münger, 2008). More recent clinical evidence suggests other biological agents, including specific bacteria, flukes, and worms, contribute to the onset of various cancers (IARC, 2013).
More than a century ago, the Nobel laureate Élie Metchnikoff pioneered our understanding of the immune system and advocated the importance of lactobacilli in health. As the scientific community continues to expose the potential health value of specific strains of lactic acid bacteria, it should not be surprising that selected viruses may represent novel interventions against some types of cancer. This form of immunotherapy, also known as oncolytic virotherapy, leverages a variety of innate, attenuated, and genetically engineered antitumor properties of specific virus species, such as the measles virus (Prestwich et al., 2008; Woller et al., 2014). Oncolytic viruses are self-replicating, tumor-selective viruses that disrupt and lyse cancer cells through multiple antitumor mechanisms (Bartlett et al., 2013). Fundamentally, these viruses induce immunogenic cell death from within the infected cancer cells. There ensues a concomitant cytotoxic immune response against the tumor cells, all of which contributes to the eradication and elimination of the tumor mass.
Regardless of the approach to cancer therapy, there remain several questions pertinent to potential immunological consequences. The intended cell death of cancer cells produces an array of immunogenic and non-immunogenic challenges. For example, apoptosis, autophagic cell death, necrosis, pyroptosis, and secondary necrosis signal the release of pro-inflammatory cytokines and activation of cytotoxic proteins (Bartlett et al., 2013). These consequences emphasize the importance of maintaining a healthy immune system, which is complex, especially during periods of cancer therapy, which often contributes to immune dysfunction, immunosuppression, and inflammation.
Roger Clemens, Dr.P.H., CFS,
Chief Scientific Officer,
Horn Company, La Mirada, Calif.