Signaling Protein For Multiple Myeloma Identified, Findings May Result In New Therapeutic Target
September 12, 2007 – 9:39 pm | posted in Cancer / OncologyResearchers at Emory University’s Winship Cancer Institute are the first to discover a mechanism that plays a critical role in the multiple myeloma cell cycle and survival. Their research may result in identification of a new therapeutic target for treating multiple myeloma.
The results of the study appear in the September issue of Cancer Cell. Jing Chen, PhD, assistant professor of hematology and oncology at Emory Winship and a Georgia Cancer Coalition Distinguished Cancer Scholar, is senior author on the paper. Sumin Kang, PhD, a postdoctoral fellow at Emory Winship, is the paper’s first author.
Multiple Myeloma is among the most common hematologic malignancies in patients over 65. About15 percent of multiple myeloma patients harbor a genetic abnormality called “t(4;14) chromosomal translocation” that causes over-expression of a tyrosine kinase called fibroblast growth factor receptor 3 (FGFR3).
Tyrosine kinases are molecules that act as biological switches inside cells, regulating processes including cell division and growth. Abnormal kinases have been identified as a driving force in many forms of cancer.
“We are interested in how FGFR3 mediates transforming signals,” says Dr. Chen. “We wanted to know which protein factors in cells are activated by FGFR3 and then transform normal cells to highly malignant cells. We identified Ribosomal S6 kinase 2 (RSK2), which is a protein factor that mediates signaling in cells as critical in downstream signaling of FGFR3 in myeloma cells.”
Dr. Chen and his colleagues are the first to discover a mechanism to “turn-on” RSK2 by FGFR3. FGFR3 impacts downstream proteins through phosphorylation at special “tyrosine” sites.
“We found that FGFR3 directly phosphorylates RSK2, which is a critical step in the process to activate (turn-on) RSK2,” says Dr. Chen.
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