Sligh and colleagues were surprised to find a panel of mitochondrial DNA deletions in the tumor-free skin that was adjacent to the tumors, but not in the tumors themselves. The tumor samples were more likely to have full-length mitochondrial DNA, with point mutations rather than significant deletions, Sligh said.
The mitochondrial DNA mutations in the tumor-free skin correlated with the aging process, Sligh said. The newly identified deletion mutations will now go into "Mitomap," a database of all known human mitochondrial genome changes.
"Unraveling the molecular clues as to why aging cells function differently than young cells requires that we have molecular markers that we can track," Sligh said. "It won't be long before other investigators who have other human tissue specimens -- brain, lung, heart, for example -- look for these changes and report back.
"It will be interesting to see if the mitochondrial DNA mutations we've found are markers of aging in other tissues or if they are specific to tissues exposed to ultraviolet light."
Either way, the newly identified biomarkers will provide another tool for studying mitochondrial damage that contributes to aging and cancer, and for screening compounds that prevent or reverse the process, Sligh said.