Scientists have detected a molecular "hot spot" that is strongly linked to liver cancer, one of the most common and lethal malignancies in the world. The spot is a tiny region of a single gene where toxins that infiltrate the liver seem to home in, sabotaging the gene and touching off cancerous growth.
The discovery, which is reported in two papers appearing today in the journal Nature, is the first persuasive example yet found of the exact way toxins and other risk factors attack DNA, the basic genetic material in cells, and cause cancer.
The finding may signal the start of what Dr. Stephen H. Friend of Massachusetts General Hospital in Charlestown, Mass., who helped bring the two research teams together, calls "molecular forensics," the ability to attribute a particular cancer unequivocally to a particular cancer-causing agent.
Right now, attempts to link, say, lung cancer to cigarettes are largely based on statistical evidence rather than molecular proof.
"The key question in cancer research has been how mutations are induced" by toxins in the environment, said Dr. Bert Vogelstein of the Johns Hopkins University.
"This is the first report I know showing a convincing demonstration that specific environmental factors induce specific mutations in cancer."
In the latest work, researchers from the National Cancer Institute in Bethesda and Massachusetts General Hospital said two risk factors already implicated in liver cancer seemed to damage the hot spot.
One suspected risk factor is a fungal poison called aflatoxin, which contaminates grain and other foods improperly stored in warm, moist places. Such contamination is a widespread problem in humid regions like sub-Saharan Africa and parts of the Far East, precisely the regions where liver cancer abounds.
The second risk factor is a poisonous chemical byproduct of the hepatitis B virus, a microbe that infects many people in developing nations where liver cancer is most prevalent.
But scientists cautioned that many experiments remained to be performed before they could be sure that either or both types of toxin caused the flaw they detected.
"The data are compelling and seem more than coincidental, but we're still in the speculating stage," said Dr. Mehmet Ozturk of Massachusetts General, the main author of one of the papers. "We must still demonstrate a direct role."