Abstract
Mitochondrial (mt) contribution to carcinogenesis has been critically discussed with circumstantial evidence against as well as for a causal role. Proliferating cancer cells are dependent on sufficient energy supply that would argue against defective mitochondria in tumor cells. On the other hand, mitochondria are the main endogenous source of reactive oxygen species as highly mutagenic side products of oxidative phosphorylation (Fridovich, 2004) and increased amounts of mtDNA mutations have been detected in a variety of tumors (reviewed by Berneburg et al., 2006).
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