Entry Date:
July 21, 1999

Glioblastoma

Principal Investigator David Housman


We have focused on the receptor tyrosine kinase, c-Ros, which we have shown to be activated in a novel manner in glioblastoma. Through the characterization of a microdeletion on 6q22 in a glioblastoma, c-Ros can be activated via fusion to a novel Golgi apparatus-associated protein. The fused protein product displays intrinsic kinase activity and is a potent oncogene. The transforming potential of the Fig-Ros fusion product resides in its ability to interact with and become localized to the Golgi apparatus. We are currently exploring the mechanisms by which a Golgi localized activated oncogene can cause cell transformation, and are initiating studies to identify small molecules which may serve as probes for Ros function in glioblastoma and the basis for possible therapeutic intervention for this tumor.