Forget cigarette smoking (well, not completely). The really bad news, says Leona Samson, is that by virtue of the act of living, a human body will be exposed to destructive threats from the environment, and from within itself. Charbroiled burgers, sunlight, pollution, and even how our bodies use oxygen all pose what Samson calls “insults” to the DNA of our cells.

Our success in fending off these inevitable DNA-damaging agents in the environment depends a lot on inheritance, Samson tells us. For instance, victims of the rare disease Xeroderma pigmentosum don’t have the capacity to repair DNA that’s been corrupted by UV radiation from the sun. Children with Xeroderma pigmentosum develop skin cancers. In the larger population, such cancers tend to occur much later in life. The reason, Samson says, is that most of us have a formidable array of mechanisms within our cells for detecting and mending defective DNA. Cells with flawed DNA that goes unrepaired must either die, or go on to mutate in often dangerous ways.

Samson wants to figure out how to protect cells against carcinogenic effects in the environment, and whether a tumor cell will be susceptible to treatment. She has been painstakingly studying the Saccharomyces cerevisiae yeast organism, trying to identify all the factors that determine whether or not DNA damaging agents kill or mutate cells. She interrogated each of this organism’s 5,800 genes, “asking one by one, which of you is making a product that’s important to helping a cell recover from damage.” In what was a “huge surprise,” Samson learned that there are more than 2,000 gene products involved in helping a yeast cell repair itself, “from areas of the cell never suspected before for being important” in this way. Now Samson must elucidate the complex cellular pathways that “talk to each other” when DNA is damaged -- and figure out “how to extend to humans, ultimately.”