The potential pathogenetic significance of mitochondrial DNA (mtDNA) mutations in tumorigenesis is controversial. We hypothesized that benign tumorigenesis of a slowly replicating tissue like the human parathyroid might constitute an especially fertile ground on which a selective advantage conferred by mtDNA mutation could be manifested and might contribute to the oxyphilic phenotype observed in a subset of parathyroid tumors.
Center for Molecular Medicine, University of Connecticut School of Medicine, 263 Farmington Ave, Farmington, Connecticut 06030-3101, USA. costa@nso2.uchc.edu
