Identification of mutations in fibroblast growth factor receptor 4 (FGFR4) that are associated with Rhabdomyosarcoma tumors; may be used to identify candidates for treatment with an FGFR4 inhibitor as an adjuvant to standard anticancer therapy.

Rhabdomyosarcoma (RMS) is the most common type of pediatric soft tissue sarcoma. Most children (>70%) with the disease die at higher stage (metastatic disease).

 

Researchers at NIH have identified mutations in fibroblast growth factor receptor 4 (FGFR4) that are associated with RMS tumors. It is proposed that individuals with FGFR4 mutations may have an increased risk for tumor metastasis. The identified FGFR4 variants can be used to identify individuals who may benefit most from treatment with an FGFR4 inhibitor as an adjuvant to standard anticancer therapeutics to decrease the risk of tumor metastasis.

 

Available for licensing are methods for identifying candidates for treatment with an inhibitor of FGFR4 by determining the presence of at least one FGFR4 variant, kits for identifying said candidates, and methods for identifying compounds that induce tumor cell death or that inhibit tumor growth or metastasis.

 

Applications:

• Potential new method for treatment of Rhabdomyosarcomas (RMS).
• Potential new method to prepare kits to diagnose activating mutations in FGFR4.
• These mutations can be used in laboratory settings to screen thousands of compounds for more specific FGFR4 gene inhibitors.
• FGFR4 is also a potential target for lung and breast cancer.
• FGFR4 monoclonal can be developed to target RMS tumors.

 

Early Stage

U.S. Provisional Application No. 61/044,875 filed 14 Apr 2008 (HHS Reference No. E-175-2008/0-US-01)

 

Inventors:

Javed Khan et al. (NCI)

 

Licensees Sought:

Available for exclusive and non-exclusive licensing.

 

Collaborative Research Opportunity:

The National Cancer Institute, Pediatric Oncology Branch, is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize Over-expression and Mutation of a Tyrosine Kinase Receptor FGFR4 in Tumors.  Please contact John D. Hewes, Ph.D. at 301-435-3121 or hewesj@mail.nih.gov for more information.