In a collaborative research with Washington University School of Medicine in St. Louis, researchers at the Translational Genomics Research Institute (TGen) discovered that introducing a particular inhibitor drug can turn "off'' receptors responsible for the growth of tumors in a significant number of patients with endometrial cancer.
They also found that the inhibitor drug proved quite beneficial even in cancer tumours containing a commonly occurring mutant gene, PTEN, earlier linked with resistance to drug treatment.
The scientists will start a clinical trial based on this study within the next year.
Led by Dr. Pamela Pollock, an associate investigator in TGen's Cancer and Cell Biology Division and the paper's senior author, the study used the latest genome-scanning technology to sequence 116 endometrioid endometrial tumor samples.
Earlier in 2007, the researchers announced that they had discovered previously unrecognized alterations in the fibroblast growth factor receptor 2 (FGFR2) gene.
It is found in the cancer cells of nearly 15 percent of women with endometrioid endometrial tumors. Such tumours represent 80 percent of all endometrial cancers.
Thus, they introduced a commercially available inhibitor drug, PD173074, and showed that they could stop the growth of tumors, and even kill cancer cells, in cases where the tumors contained the altered FGFR2 gene.
The altered gene causes the receptors to get stuck in the "on'' position and signal the endometrial cells to grow out of control.
"These findings could accelerate the development of new treatments for endometrial cancer because there are already drugs in clinical trials that inhibit FGFR2 function,'' Pollock said.
The new findings appear in a paper published as a priority report by Cancer Research, a Philadelphia-based peer-reviewed journal dedicated to original cancer research.