NEW YORK, May 16, 2012 Researchers at NYU School of Medicine have identified a target for slowing the progression of multiple myeloma by using currently available drugs.
Published recently in Nature Cell Biology, the study reveals a pathway that, if deactivated, may help slow the development of the disease.
"We have the ability to target this pathway with drugs that already exist," said lead investigator Michele Pagano, MD, the May Ellen and Gerald Jay Ritter Professor of Oncology in the Department of Pathology and a member of the NYU Cancer Institute at NYU Langone Medical Center, and a Howard Hughes Medical Institute investigator. "Many other lymphomas are also controlled by this pathway, so while we're optimistic that this discovery will provide a way to kill multiple myeloma cells, we're also very hopeful that this can be applied to other lymphomas and that it will have a major impact on these aggressive cancers."
Pagano and colleagues put together several new pieces of the puzzle surrounding the survival and spread of multiple myeloma cells and the Nuclear Factor kappa B (NF-кB) pathway. This complicated pathway induces transcription of genes that control inflammation, immunity, and certain developmental processes. It is also known to frequently be involved in disease.
In normally functioning cells, the NF-кB pathway turns off and on, triggered by the accumulation and then degradation, or breakdown, of a protein called p100. When the pathway is "on," p100 is degraded, allowing for pathway-dependent gene transcription. Several hours after the pathway's activation, p100 begins to accumulate in the cell's nucleus, naturally blocking the pathway, so that the gene transcription signal is temporarily blocked and transcription is halted.
In lymphomas, including multiple myeloma, however, the NF-кB pathway remains active, providing a refuge for lymphoma cells to hide. In fact, within this a
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NYU Langone Medical Center / New York University School of Medicine