If you're a smoker, you could spend just half an hour talking with Oliver Hankinson, and you might reconsider your habit. If you like the occasional well-cooked burger, you might reconsider that choice, too.
Hankinson, a molecular toxicologist at the University of California at Los Angeles, has devoted 35 years to studying how toxins cause disease—specifically cancer. The AAAS Fellow's conclusions come from a series of discoveries about how toxins in cigarette smoke and the chemical compound dioxin disrupt the functioning of cells. He has focused on dioxin, a byproduct of industrial processes, and benzo(a)pyrene, which is found in smog, cigarette smoke and overcooked food.
At the UCLA Medical School, Hankinson, professor of pathology and laboratory medicine, tells first-year medical students that cancer is largely a disease of lifestyle.
"I say that 80 percent of cancers in the human are caused by environmental agents," he said. "Tobacco: 30 percent. Diet: 30 percent. Industrial pollution is not as important as was once thought."
His office sits at the end of a corridor plastered with "Biohazard\ stickers. But there's nothing of the alarmist in Hankinson's manner: He describes his discoveries in calm, measured tones over a cup of tea.
In the early 1990s, Hankinson cloned a gene called ARNT. It is part of a complex that interacts with a protein-coding gene called AHR. The interaction allows cells to enhance the effects of toxins or to change the expression of genes that combat toxins.
"Usually," he said, \"turning on those genes is trouble. Certainly, people are trying to prevent their being turned on."
Since then, a body of research has emerged that shows how ARNT and AHR interact to cause cancer.
Hankinson's group, in collaboration with researchers at Oxford, was the first to show that ARNT, when complexed with another gene, is required for a cell's response to hypoxia—a deficiency of oxygen. Subsequent work by others has shown that chemical exposure can compromise this protection against loss of oxygen.
Hankinson, who grew up in Brighton on the south coast of England, started out studying microorganisms, but his interest turned to human genetics in 1970 while studying for his Ph.D. at Cambridge University. He heard the late Frank Ruddle, a pioneer in genetic engineering at Yale University, speak at a biochemistry meeting, and was intrigued by the idea that someone could map human genes.
"It was mind-boggling to me," Hankinson said.
In 1976, during a postdoctoral post at the University of California at Berkeley, he received his first grant from the National Institutes of Health. For the next 30 years, his lab employed as many as 10 scientists at a time. Their pictures fill two bulletin boards in his office—from faded snapshots of young people with long hair and loose clothing to recent computer printouts with orderly mug shots of well-coiffed students.
The lab is quieter these days. One year ago, the last of the grants expired. In recent months, Hankinson has worked with a visiting scientist, Sara Huerta-Yepez, but she is returning to Mexico soon. Hankinson is conducting his own experiments now and is pleased with the results.
"I've enjoyed it more than anything in the last 25 or 30 years," he said. "One day, you do an experiment, and the next day, you see if it worked."
His current research is delving into molecular interactions that govern tumor growth in cells. He is finding that carcinogenesis by dioxin can be increased or decreased depending on the particular fat content of a mouse's diet.
"What you ingest will have an effect on carcinogenesis," he said. But those effects are not clear-cut. The trouble caused by one substance can be countered by another. "The whole diet story is a very, very messy story. You've got to look at the whole diet," he said.
Hankinson also is turning his attention to the next frontier of the field, which involves determining an individual's genetic susceptibility to the effects of carcinogens.
"Ultimately," Hankinson said, \"we may be able to determine a profile of people's susceptibility."