NEW YORK (May 13, 2013) -- A soon-to-be-tested class of drug inhibitors were predicted to help a limited number of patients with B-cell lymphomas with mutations affecting the EZH2 protein. However, a research team, led by investigators at Weill Cornell Medical College, now report that these agents may, in fact, help a much broader cross section of lymphoma patients.
The study, reported in Cancer Cell, found that the EZH2 protein the drug agents inhibited is a powerful regulatory molecule in B-cells, and a key driver of cancer in these immune cells.
The study's lead investigator, Weill Cornell Medical College's Dr. Ari Melnick, suggests that combining an EZH2 inhibitor with another related targeted therapy may offer a much improved treatment for follicular lymphoma, a cancer that currently has no cure, as well as a non-toxic alternative to chemotherapy for at least a third of diffuse large B-cell lymphomas. Because these two lymphomas account for 70 percent of adult lymphomas, Dr. Melnick believes the new therapy could potentially help a broad cross section of lymphoma patients.
"Our research indicates that these inhibitors will be remarkably effective. I am very optimistic," says Dr. Melnick, the Gebroe Professor of Hematology/Oncology, professor of medicine and director of the Raymond and Beverly Sackler Center for Biomedical and Physical Sciences at Weill Cornell. "Researchers had thought EZH2 inhibitors would only help patients with a mutation in their EZH2 gene, which represents a small subset of lymphoma patients. What we found is that a majority of lymphomas turn out to be dependent on normal EZH2, not just mutated EZH2."
Tumor Cells Depend on the EZH2 Master Regulator
The new study was aimed at understanding what normal as well as mutated EZH2 does within B-cells -- basic information that remained unknown despite more than a decade of research into the protein.
The role of B-cells (
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Weill Cornell Medical College