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Event Title

The Connection Between the Spontaneous Regression Seen in Neuroblastomas, Hypertumors, and Reactive Oxygen Species

Date

April 2021

Location

Online

Description

This paper postulated that there is a correlation between neuroblastomas, which exhibit characteristics of hypertumors, and metabolic pathways to explain Peto’s Paradox. The phenomenon that larger animals have decreased rates of cancer despite having an increased number of dividing cells, which should theoretically lead to increased cancer rates, is Peto’s Paradox. Hypertumors are theorized to be cheater cells that develop and proliferate within a pre-existing tumor, depleting the original tumor’s resources and blood supply. Neuroblastomas exhibit characteristics seen in hypertumors including spontaneous non-apoptotic cell death and overexpression of the RAS g-protein. Studies have shown a correlation between the activation of the JNK and p38 MAPK pathways in KP-N-TK (neuroblastoma) cells in an ROS- dependent manner and the anticancer drug N-HPR (Fenretinide). Metabolism, the second hypothesized explanation for peto’s paradox, affects ROS levels which have also been linked to apoptotic cell death by inducing free radical formation. This is hypothesized to be another possible mechanism of fenretinide. The purpose of this review is to highlight the cellular mechanisms involved in the aforementioned connections. This suggests the existence of hypertumors which ultimately can be used to limit the progression of cell growth in Neuroblastomas.

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Presentation

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The Connection Between the Spontaneous Regression Seen in Neuroblastomas, Hypertumors, and Reactive Oxygen Species

Online

This paper postulated that there is a correlation between neuroblastomas, which exhibit characteristics of hypertumors, and metabolic pathways to explain Peto’s Paradox. The phenomenon that larger animals have decreased rates of cancer despite having an increased number of dividing cells, which should theoretically lead to increased cancer rates, is Peto’s Paradox. Hypertumors are theorized to be cheater cells that develop and proliferate within a pre-existing tumor, depleting the original tumor’s resources and blood supply. Neuroblastomas exhibit characteristics seen in hypertumors including spontaneous non-apoptotic cell death and overexpression of the RAS g-protein. Studies have shown a correlation between the activation of the JNK and p38 MAPK pathways in KP-N-TK (neuroblastoma) cells in an ROS- dependent manner and the anticancer drug N-HPR (Fenretinide). Metabolism, the second hypothesized explanation for peto’s paradox, affects ROS levels which have also been linked to apoptotic cell death by inducing free radical formation. This is hypothesized to be another possible mechanism of fenretinide. The purpose of this review is to highlight the cellular mechanisms involved in the aforementioned connections. This suggests the existence of hypertumors which ultimately can be used to limit the progression of cell growth in Neuroblastomas.