Michael Rodio | Dec. 3, 2013 | Harper Cancer Research Institute
Cancer’s origin point—a human gene gone haywire—is, in many cases, also its weak spot. If you could block the abnormal function of a gene that is important for metastasis, the theory goes, then maybe you can stop cancer from spreading.
But there’s a catch—hit the weak spot with too much force, and you could trigger a cascade of side effects that may be as bad as the original cancer.
In her research, Tracy Vargo-Gogola, assistant professor of biochemistry & molecular biology at Indiana University School of Medicine-South Bend and adjunct assistant professor of biological sciences at the University of Notre Dame, faces this problem every day. Vargo-Gogola, a breast cancer researcher at the Harper Cancer Research Institute, studies a gene called CDC42. The CDC42 gene is overactive in a type of breast cancer called invasive ductal carcinoma, which comprises 75 to 80 percent of breast cancers. CDC42 is active in other types of cancers as well.