Peto’s Paradox is defined as the lack of correlation between larger animals and cancer risk. Under the assumption that all cells have equal risk of becoming cancerous, larger animals should have greater rates of cancer. However, the inverse is true. Determining the cause of this variation may allow a supplemental approach to cancer treatment. A combination of two reasons may account for this correlation including hypertumors and metabolism. Hypertumors, or cheater cells, are hypothesized to suppress cancer growth through spontaneous autophagic degradation and overexpression of the RAS g-protein. Both of these characteristics are exhibited in Neuroblastomas. An anticancer drug used on KP-N-TK (Neuroblastoma) cell lines exhibited cell death that would be seen in hypertumors through activation of the JNK and p38 MAPK pathways in an ROS- dependent manner. Varying effects of ROS levels are explained by the theory of metabolism including elevated levels triggering apoptosis as seen in Fenretinide. The purpose of this review is to highlight the cellular mechanisms of ROS and Neuroblastomas treated with Fenretinide. This suggests the existence of hypertumors through metabolic means which ultimately can be used to maintain the progression of cell growth in Neuroblastomas.
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