Wild-type and pediatric GISTs, which often do not respond to this therapy, showed higher levels of IGF1R.
Excess amounts of a protein called IGF-1R in patients with gastrointestinal stromal tumors (GISTs) could indicate that the patient would be less responsive to the drug imatinib mesylate, known as Gleevec, according to researchers at the Fox Chase Cancer Center.
In most occurrences, GISTs develop through a mutation in the genes c-KIT or PDGFRA, both of which are targets of Gleevec. GISTs without those mutations, known as wild type, as well as pediatric GISTs do not often respond well to treatment with Gleevec.
The Fox Chase researchers found that when compared to mutant GISTs, the DNA of wild type and pediatric GISTs exhibited more copies of the IGF1R gene. These tumors also produced many more copies of the IGF-1R protein, which promotes cell survival, proliferation, and growth in normal cells and tumors. In the laboratory, the researchers found that drugs that decrease IGF-1R activity induced the death of tumor cells.
Andrew K. Godwin, Ph.D., director of Fox Chase’s clinical molecular genetics laboratory will presents these findings at the “2008 Annual Meeting of the American Society of Clinical Oncology,” which will be held May 30 through June 3.