In order to determine the role of mitochondrial DNA mutations in thyroid tumorigenesis, Abu-Amero et al. (2005a) sequenced the entire mtDNA from 24 thyroid tumor specimens and four thyroid cancer cell lines.  Somatic mutations were identified in 37% of primary thyroid carcinomas (PTC) and among 25% of multinodular hyperplasia cases.  Most mutations were nucleotide substitutions resulting in missense mutations.  Of these mutations, 14 were nonsynonymous and 36 were synonymous.  A novel 9948.G>A nonsynonymous mutation was detected in the CO3 gene.  Also, three synonymous variants were found in both PTC and control samples, one was novel.  In a separate study, Abu-Amero et al. (2005b) sequenced the entire mitochondrial coding region for a 70 year-old man with non-arteriticanterior ischemic optic neuropathy.  A single homoplasmic mutation transition at mtDNA nt-9957 was found; resulting in Phe251Leuc amino acid change in the C- terminus of the cytochrome c oxidase subunit III polypeptide.  Phenylalanine at position 251 is a highly conserved amino acid among species, changes in this amino acid cause inhibition in complex III activity.  Abu-Amero and Bosley (2006) studied further the molecular and biological characteristics of mitochondria in patients with Leber hereditary optic neuropathy (LHON)-like optic neuropathies.  Thirty five patients (21 males and 14 females) and 159 matched controls from Saudi Arabia were included in this study.  Forty one non-synonymous mtDNA sequence variants were identified in LHON patients; 14 were pathogenic.  Of these variants, 21 were in complex I, seven in complex III, five in complex IV, six in complex V, one in tRNA glutamine, and one in 12S rRNA.  Similar to previous reports on mutation association with LHON, these mtDNA changes were transitions.  Two variants were found within the MT-CO3 gene: A9660C and A9667G.  The A9660C variant was thought to be probably pathogenic