The maintenance of mitochondrial genetic stability is crucial during the oncogenic process.

The main energetic resources of the cell are the mitochondria. As such, these organelles control a number of processes related to the life and death of the cell and also have a prominent function in the maintenance of tumor cells. In the last years, several authors have proposed an active role for mitochondria in tumorigenesis, more specifically concerning somatic mutations in mitochondrial DNA (mtDNA). Here, we wanted to evaluate this hypothesis based on the conclusions obtained in a model of gliomagenesis with elevated levels of ROS (reactive oxygen species), a toxic by-product of tumor metabolism. According to our findings, none of the mtDNA variants were found relevant to the tumoral process or suggest the involvement of mitochondria in tumorigenesis beyond the metabolic requirements of the tumoral cell. We conclude that there is not enough evidence to support the claim that mitochondrial instability holds any relevant role in the tumoral process.