STUDY PINPOINTS LIKELY START OF BURKITT'S LYMPHOMA

June 20, 1994
Media Contact:Joann Rodgers
Phone: (410) 955-8659
E-mail: JRodgers@welchlink.welch.jhu.edu

A team of researchers from Johns Hopkins, Columbia University and the National Cancer Institute has uncovered what is probably the main way normal cells become malignant in Burkitt's lymphoma, a cancer of the immune system The process may also be a key step in switching on cancers of the breast and colon.

"We believe our discovery could be a significant part of a general process -- and one that's been overlooked -- that causes tumors to form" says Hopkins hematologist Chi Van Dang, M.D., Ph.D., part of the team whose research was published in the April 8 issue of Science.

While the discovery of any new pathway in cancer offers targets for future therapy, the immediate clinical benefit of the discovery, Dang says, "may be insight into how aggressive a tumor is. It also gives us some idea how tumors start on a molecular level.'l

Burkitt's lymphoma is common in central Africa, most frequently striking children and causing large tumors in the abdomen or the jaw. Early stages respond well to chemotherapy, but left alone, it progresses rapidly and is fatal. Burkitt's lymphoma is not common in the United States.

The research centers on a gene called m common to all cells. Normally, myc plays a role in controlling cell division; scientists measure surges in myc activity just before cells begin to copy their genetic material, Dang says. Then the activity drops. 'We know myc must be important because there are at least two other systems in the cell to control it," he adds.

Yet in cancers such as Burldtt's lymphoma, cells behave as though the myc gene is permanently switched on.

What the researchers found may happen is this: when the myc gene is normal, it produces a protein that switches on cell division. In cells that aren't dividing, that protein is suppressed by another molecule, plO7 -- a biological wet blanket. The researchers confirmed this using genetically engineered cell cultures containing isolated myc genes and plO7.

"What goes wrong, we believe, is that many Burkitt's lymphoma cases have mutations in the myc gene. These produce an abnormal protein that can't be suppressed by plO7," says Dang. The result is the uncontrolled growth that characterizes cancer.

"We were really surprised how common these mutations were in Burkitt's lymphoma. More than 70 percent of the cases had myc mutations," says Dang.

"Until now," Dang says, "people assumed that things went wrong because extra copies of the myc gene or breaks in chromosomes moved myc away from neighboring genes that regulated it." But we also knew that, in breast cancer, for example, chromosomes containing the myc gene appear to be normal 70 percent of the time. From our study, we now know to investigate mutations within the myc gene.

"This suggests a general mechanism that no one's looked for in other cancers," he adds. Other researchers in the study are Wei Gu and principal investigator Riccardo DaRa-Favera, of Columbia University, New York; and Kishor Bhatia and Ian Magrath, of the National Cancer Institute, which funded the study.


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