Wood, a native of Colorado, has been studying DNA repair genes since 1978. He earned his doctorate in biophysics in 1982 at the University of California, Berkeley, and after a post-doctoral fellowship at Yale University joined the Imperial Cancer Research Fund in 1985. Dr. Ronald Herberman, director of the University of Pittsburgh Cancer Institute, said Wood was hired to fill the Cyert chair after a two-year international search. The impact of deficient DNA repair genes can be profound, Wood noted. He has done extensive research on xeroderma pigmentosa, a disease in which a set of genes for a type of DNA restoration called nucleotide excision repair are deficient.
Patients are vulnerable to ultraviolet light, developing painful blisters and sunburn.
They face a 1,000-fold increase in skin cancer incidence, he said, with many children developing cancers by age 5. Subtler effects are emerging from genome data. In the case of a gene called XRCC1, for instance, people who have one of two or three common variants of the gene seem to be at higher risk of genetic damage from tobacco, as well as age-related DNA damage. In most cases, however, scientists still don't know which of these variant spellings of genes are important. Many anti-cancer drugs work by damaging DNA and researchers have become convinced that some tumors survive because they have unusually effective DNA repair mechanisms.