Researchers identify cause of aggressive childhood cancer

Researchers have generated a mouse model of a new type of tumor suppressor gene that triggers a rapidly advancing cancer that affects children. The discovery of the fast-onset cancers that result from inactivation of the gene and the technique used to generate the model will likely prove useful in studying genes involved in other forms of cancer.

The research team, which was led by Howard Hughes Medical Institute investigator Stuart H. Orkin, and former HHMI physician postdoctoral fellow Charles Roberts, reported its findings in the November 2002 issue of the journal Cancer Cell. Orkin and Roberts are at the Dana-Farber Cancer Institute, Children's Hospital, Boston, and Harvard Medical School.

The tumor suppressor gene, called SNF5, codes for a protein that is a component of a large complex called SWI/SNF that attaches to chromatin to regulate the expression of genes. Chromatin is the complex of DNA and proteins in the nucleus of the cell.

"There has been indirect evidence that some types of chromatin remodeling complexes might play a role in cancer," said Roberts. In a key finding reported in 1998, French researchers showed that mutations that inactivated SNF5 were present in tissue samples from children with malignant rhabdoid tumors. "That's what first caught our interest, that we might be dealing with a new type of tumor suppressor," said Roberts. Malignant rhabdoid tumors are rare but highly aggressive cancers that usually appear in infancy. These tumors are resistant to treatment and usually cause death within a year of diagnosis.

With the initial evidence that SNF5 was involved in such tumors, Roberts, Orkin and their colleagues set out to establish in mice that loss of SNF5 did indeed produce cancers. The problem, said Roberts, was that the usual methods for knocking

Contact: Jim Keeley
Howard Hughes Medical Institute

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